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Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models
Open accessAbstract
The goal of this review is to discuss how behavioral tests in mice relate to the pathological and neuropsychological features seen in human Alzheimer's disease (AD), and present a comprehensive analysis of the temporal progression of behavioral impairments in commonly used AD mouse models that contain mutations in amyloid precursor protein (APP). We begin with a brief overview of the neuropathological changes seen in the AD brain and an outline of some of the clinical neuropsychological assessments used to measure cognitive deficits associated with the disease. This is followed by a critical assessment of behavioral tasks that are used in AD mice to model the cognitive changes seen in the human disease. Behavioral tests discussed include spatial memory tests [Morris water maze (MWM), radial arm water maze (RAWM), Barnes maze], associative learning tasks (passive avoidance, fear conditioning), alternation tasks (Y-Maze/T-Maze), recognition memory tasks (Novel Object Recognition), attentional tasks (3 and 5 choice serial reaction time), set-shifting tasks, and reversal learning tasks. We discuss the strengths and weaknesses of each of these behavioral tasks, and how they may correlate with clinical assessments in humans. Finally, the temporal progression of both cognitive and non-cognitive deficits in 10 AD mouse models (PDAPP, TG2576, APP23, TgCRND8, J20, APP/PS1, TG2576 + PS1 (M146L), APP/PS1 KI, 5×FAD, and 3×Tg-AD) are discussed in detail. Mouse models of AD and the behavioral tasks used in conjunction with those models are immensely important in contributing to our knowledge of disease progression and are a useful tool to study AD pathophysiology and the resulting cognitive deficits. However, investigators need to be aware of the potential weaknesses of the available preclinical models in terms of their ability to model cognitive changes observed in human AD. It is our hope that this review will assist investigators in selecting an appropriate mouse model, and accompanying behavioral paradigms to investigate different aspects of AD pathology and disease progression.
Overview
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Written from the paper’s full text.
TL;DR
This review maps how behavioral tasks used in amyloid precursor protein (APP) mutant mice correspond to the neuropsychological assessments used clinically in Alzheimer's disease (AD), and tabulates the temporal onset of cognitive and non-cognitive deficits across 10 commonly used AD mouse models. It concludes that no single model recapitulates human AD, but that most models show spatial working memory deficits earlier than deficits in other cognitive domains.
Key findings
- Across the reviewed models, the earliest observable cognitive impairment is consistently in spatial working memory (assessed by water maze tasks), generally followed by associative learning/reference memory deficits, with recognition memory deficits appearing later (e.g., PDAPP: working memory at 4 months, NOR at 6 months; Tg2576: spatial working memory at 5 months, NOR at 12 months; APP/PS1 KI: RAWM at 9 months, recognition memory at 15 months).
- Onset varies substantially by model: J20 shows recognition memory deficits earliest (1–2 months), while APP/PS1 KI shows the latest onset (7–9 months for earliest deficits).
- Non-cognitive abnormalities are also present in most models, including increased locomotor activity (J20 and TgCRND8 earliest at ~1 month; PDAPP and Tg2576 at ~3 months; PS1, 3×Tg-AD, and APP23 at ~6–9 months), anxiety, circadian/sleep disruption, and aggression (e.g., APP23 aggression by 6 months).
- The review notes that increased aggression presents in as much as 65% of AD patients, and that depressive symptom prevalence in AD is reported to range from 2% to 85%, though little work has examined depressive-like behavior in AD mouse models.
Methods
- Narrative review, not primary experimental work: it summarizes human AD neuropathology (ABC scoring of Amyloid, Braak, CERAD), clinical neuropsychological instruments (MMSE, MoCA, SBT, ADAS-cog, Logical Memory I/II, BVRT), and mouse behavioral tasks (MWM, RAWM, Barnes maze, Y-/T-maze, NOR, fear conditioning, passive/active avoidance, DMTP/DMTS, 3- and 5-CSRTT, set-shifting, reversal learning, WWWhich).
- The core synthesis is two tables (Table 3 for five APP models: PDAPP, TG2576, APP23, TgCRND8, J20; Table 4 for five APP+PS1/Tau models: APP/PS1, TG2576+PS1(M146L), APP/PS1 KI, 5×FAD, 3×Tg-AD) coding impairment, no impairment, or no data by age, with an asterisk marking first appearance of diffuse amyloid plaques.
- No new data, sample sizes, or statistical analyses are reported; findings are drawn from cited primary studies.
Limitations
- Stated by the paper: no animal model recapitulates the entirety of AD; most models represent familial AD (FAD), which accounts for only a small percentage of total AD cases; background strain and likely overexpression of mutant human APP genes on brain development and function must always be considered; language-dependent domains (verbal acuity, verbal recall) cannot be modeled in rodents; the WWWhich episodic-like memory task is not comparable to human episodic memory tests because those rely on language; homology between rodent and human 5-CSRTT is "far from perfect."
- Stated by the paper: the tables are not an all-encompassing list of mouse models, only examples of commonly used APP-mutation models.
- Evident from the text: the tables contain many cells with no available data, and the review documents inconsistent reports across studies for several models (e.g., Tg2576 spatial memory deficits not replicated in some reports; PDAPP recognition memory findings inconsistent), indicating that model-by-model progression claims rest on heterogeneous and sometimes conflicting literature.
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In the paper
“Similar to the reported activity disturbances, circadian rhythm disruptions are also observed in many of the AD mouse models”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Circadian rhythm and sleep disruptions
What the sources say
- Not checked yetcites Huitron-Resendiz et al., 2002
- Not checked yetcites Vloeberghs et al., 2004
- Not checked yetcites Wisor et al., 2005
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Other models such as the TG2576 develop the anxiety-like disturbances later at the age of 9–11 months of age”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
What the sources say
- Not checked yetcites Gil-Bea et al., 2007
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“not all murine AD models exhibit anxiety disturbances”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
What the sources say
- Not checked yetcites Arendash et al., 2001b
- Not checked yetcites Lalonde et al., 2002
- Not checked yetcites Webster et al., 2013
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Many AD mouse models also display increased aggressive behavior”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Moechars et al., 1996
- Not checked yetcites Van Dorpe et al., 2000
- Not checked yetcites Ambree et al., 2006 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Several mouse models of AD also display sleep disruption.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Circadian rhythm and sleep disruptions
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“These aggressive disruptions appear to develop later than the onset of cognitive deficits in this model”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Kelly et al., 2003
- Not checked yetcites Van Dam et al., 2003
- Not checked yetcites Vloeberghs et al., 2006
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Anxiety disturbances have been reported in many of the AD mouse models”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
What the sources say
- Not checked yetcites Moechars et al., 1996
- Not checked yetcites Lalonde et al., 2003
- Not checked yetcites Gil-Bea et al., 2007
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Still, the majority of models do display these disturbances”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“The APP23 mouse model of AD also shows increased aggressive behaviors”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Vloeberghs et al., 2006
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The temporal time course of these anxiety-like disturbances can vary depending on the mouse model.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- It may state two separate claims as one. 41
- The quote only partly states this claim. 1
- Probably not a substantial claim. 24
None of the sources cited for this claim have been checked yet.
In the paper
“The onset of the disturbances is different for each model, with the J20 and the TgCRND8 mice developing disruptions earliest (approximately 1 month of age), followed by PDAPP and TG2576 (approximately 3 months of age), and the PS1 [Tg2576 + PS1 (M146L)], 3×TgAD, and APP23 mice developing last (approximately 6–9 months of age)”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Locomotor activity
What the sources say
- Not checked yetcites Dodart et al., 1999
- Not checked yetcites King et al., 1999
- Not checked yetcites Arendash et al., 2001b
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Other AD mouse models that show activity disturbances are the PDAPP, TG2576, J20, APP + PS1 [Tg2576 + PS1 (M146L)], and 3×Tg-AD mouse models of AD.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Locomotor activity
What the sources say
- Not checked yetcites Dodart et al., 1999
- Not checked yetcites King et al., 1999
- Not checked yetcites Arendash et al., 2001b
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“the greater the sleep disruptions are, the more severe the cognitive decline seems to be”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Circadian rhythm and sleep disruptions
What the sources say
- Not checked yetcites Huitron-Resendiz et al., 2002
- Not checked yetcites Huitron-Resendiz et al., 2005
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
In the paper
“in the TG2576 mouse increased aggressive behaviors display themselves in both the frequency of attacks on other home cage mice as well as on the latency to first attack when interacting with a novel mouse”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Alexander et al., 2011 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“in some models the behavioral disturbances start early at 1–2 months of age or 3–6 months of age for the J20 and the APP/PS1 models, respectively”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
What the sources say
- Not checked yetcites Lalonde et al., 2004
- Not checked yetcites Reiserer et al., 2007
- Not checked yetcites Harris et al., 2010
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“most of the studies using mouse models of AD have focused on understanding/correcting the cognitive deficits associated with the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Conclusions
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“NFTs spread to the limbic and medial temporal lobe (Braak stage III-IV), and this stage correlates with early AD symptoms related to memory (Schmitt et al., 2000; Riley et al., 2011).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Overview of neuropathological changes in AD
What the sources say
- Not checked yetcites Schmitt et al., 2000
- Not checked yetcites Riley et al., 2011
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Because the ADAS-cog has an excellent test-retest reliability and is considered to be one of the most sensitive scales for assessing cognitive changes related to AD (Emilien et al., 2004), this test is extensively used in AD clinical trials as an outcome measure of cognitive change (Schmitt and Wichems, 2006; Connor and Sabbagh, 2008).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Emilien et al., 2004
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Because the ADAS-cog has an excellent test-retest reliability and is considered to be one of the most sensitive scales for assessing cognitive changes related to AD (Emilien et al., 2004), this test is extensively used in AD clinical trials as an outcome measure of cognitive change (Schmitt and Wichems, 2006; Connor and Sabbagh, 2008).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Schmitt and Wichems, 2006
- Not checked yetcites Connor and Sabbagh, 2008
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The MMSE has excellent reproducibility that lends itself well to longitudinal use in tracking the progression of the cognitive impairments associated with AD (Jacqmin-Gadda et al., 1997; Aevarsson and Skoog, 2000; Chatfield et al., 2007).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Jacqmin-Gadda et al., 1997
- Not checked yetcites Aevarsson and Skoog, 2000 source
- Not checked yetcites Chatfield et al., 2007
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Another commonly used test battery is that of the Short Blessed Test (SBT) which consists of a six-item test designed to identify the cognitive dysfunction seen in AD (Katzman et al., 1983).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Katzman et al., 1983
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Despite the simplicity and brevity of the SBT, the results that it produces have demonstrated excellent reliability (Fuld, 1978).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Fuld, 1978
Strength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Similarly, the SBT was the first mental status examination to be correlated with amyloid plaque burden at autopsy (Carpenter et al., 2011).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Carpenter et al., 2011
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The Mini-Mental Status Examination (MMSE) is one of the most commonly used neuropsychological screening tools for cognitive impairments seen in AD (Simard and Van Reekum, 1999; Snyderman and Rovner, 2009).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Simard and Van Reekum, 1999
- Not checked yetcites Snyderman and Rovner, 2009
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The data also support the “Amyloid Cascade Hypothesis”(Karran et al., 2011), a deceptively complex hypothesis which posits that beta-amyloid/plaque pathology kindles widespread tau/NFT pathology, with the tau/NFT pathology constituting the more direct cause of the cell loss and synapse elimination underlying clinical disease (Nelson et al., 2009b, 2012).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Overview of neuropathological changes in AD
What the sources say
- Not checked yetcites Karran et al., 2011
- Not checked yetcites Nelson et al., 2009b
- Not checked yetcites Nelson et al., 2012
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Outside of frontotemporal lobar degeneration (FTLD), one does not see widespread cortical NFTs without abundant plaque pathology.
In the paper
“The Alzheimer's Disease Assessment Scale (ADAS) was specifically developed to measure the severity of symptoms commonly seen in AD (Rosen et al., 1984).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Rosen et al., 1984
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“These tasks rely on the natural exploratory behavior (tendency to choose an alternative arm over an arm which has been previously explored) of rodents and are considered the most rudimentary tasks to assess spatial working memory (Dudchenko, 2004).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Dudchenko, 2004
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Once the AD patient progresses past MCI and into dementia, general cognition continues to decline with deficits appearing in all respective cognitive domains (Huff et al., 1987; Locascio et al., 1995; Lambon Ralph et al., 2003; Mckhann et al., 2011).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Cognitive neuropsychological assessment summary
What the sources say
- Not checked yetcites Huff et al., 1987
- Not checked yetcites Locascio et al., 1995
- Not checked yetcites Lambon Ralph et al., 2003
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Large numbers of AD mouse models have been tested in the MWM and most show AD related cognitive deficits (Webster et al., 2013).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Webster et al., 2013
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Instead, spatial based working memory tasks are heavily employed in murine working memory testing and likely are more depictive of the visuospatial working memory tasks used clinically (Benton, 1992; Benedict and Groninger, 1994).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Benton, 1992
- Not checked yetcites Benedict and Groninger, 1994
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Working memory is perhaps one of the most well modeled aspects of the memory deficits in AD.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Some cognitive domains disrupted in AD have been extensively modeled (reference memory, working memory and executive function), some less so (attention), and some nearly not at all (episodic memory).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD?
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Other cognitive domains impaired in human AD such as those involving language (i.e., verbal acuity tasks and verbal recall tasks) simply cannot be modeled in rodent models.
None of the sources cited for this claim have been checked yet.
In the paper
“Clinically, many of the neuropsychological tests that assess working memory rely heavily on the use of verbal tasks (Kaplan et al., 1978; Benedict et al., 1998; Spreen and Strauss, 1998; Delis et al., 2000), employing language as a core construct and thus are not feasible to model using mice.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Kaplan et al., 1978
- Not checked yetcites Benedict et al., 1998 source
- Not checked yetcites Spreen and Strauss, 1998
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Other cognitive domains impaired in human AD such as those involving language (i.e., verbal acuity tasks and verbal recall tasks) simply cannot be modeled in rodent models.
In the paper
“Composite scores encompassing multiple neuropsychological tests are often used and can provide some of the most reliable assessments of global cognitive status relating to AD as well as serving as efficacy outcome measures in clinical trials (Bernick et al., 2012).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Cognitive neuropsychological assessment summary
What the sources say
- Not checked yetcites Bernick et al., 2012 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“These early deficits in episodic memory are followed closely by deficits in semantic memory, and both are developed before other deficits in cognitive domains such as attention, visuospatial memory, or executive function (Bondi et al., 2008).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Cognitive neuropsychological assessment summary
What the sources say
- Not checked yetcites Bondi et al., 2008
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Perhaps the most widely employed spatial working memory task is that of the Morris Water Maze (MWM) (Morris et al., 1982).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Morris et al., 1982
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Other common tasks of murine spatial working memory are the Radial Arm Water Maze (RAWM) and the Barnes Maze (Barnes, 1979; Diamond et al., 1999; Alamed et al., 2006).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
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None of the sources cited for this claim have been checked yet.
In the paper
“Depending on the baiting paradigm, unimpaired rats and mice will quickly learn where the food reward is and which arms have previously been visited, and will avoid re-entering a previously entered arm.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Olton and Samuelson, 1976
- Not checked yetcites Olton et al., 1979
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Response inhibition is required for the appropriate control of an individual's behavioral actions in response to a stimulus (Robbins, 1996; Humby et al., 1999; Perry and Hodges, 1999; Romberg et al., 2013a).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling executive function
What the sources say
- Not checked yetcites Robbins, 1996
- Not checked yetcites Humby et al., 1999
- Not checked yetcites Perry and Hodges, 1999
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“In many ways, set-shifting tasks are similar to the Wisconsin Card Sorting Task in that they form the gold standard for assessing executive function (Drewe, 1974; Robinson et al., 1980; Arnett et al., 1994).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling executive function
What the sources say
- Not checked yetcites Drewe, 1974
- Not checked yetcites Robinson et al., 1980
- Not checked yetcites Arnett et al., 1994 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“All of the rodent behavioral tasks discussed in this section have been specifically developed to assess deficits in cognitive domains related to what is seen in human AD.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Summary of mouse behavioral tests
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Cognitive decline is a defining feature of AD, and many mouse models have been developed that recapitulate aspects of the cognitive impairments seen in AD (Elder et al., 2010; Hochgrafe et al., 2013; Platt et al., 2013).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
What the sources say
- Not checked yetcites Elder et al., 2010
- Not checked yetcites Hochgrafe et al., 2013
- Not checked yetcites Platt et al., 2013
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, caution should be used when attempting to correlate any preclinical finding concerning episodic memory in mice to that of human cognition.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence.
None of the sources cited for this claim have been checked yet.
In the paper
“However, work over the past few decades on episodic-like memory across a number of animal species has suggested otherwise, and several mouse behavioral tasks designed at assessing episodic-like memory have been developed (Clayton and Dickinson, 1998; Clayton et al., 2001; Griffiths and Clayton, 2001; Morris, 2001; Davis et al., 2013a,b).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
What the sources say
- Not checked yetcites Clayton and Dickinson, 1998
- Not checked yetcites Clayton et al., 2001
- Not checked yetcites Griffiths and Clayton, 2001
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“This is largely because the human tasks rely on language as a foundational construct for assessment. Obviously, there exists no such component in the WWWhich task for mice.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Historically, episodic memory was thought to be unique to humans (Tulving and Markowitsch, 1998).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
What the sources say
- Not checked yetcites Tulving and Markowitsch, 1998
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“While the NOR task itself is too simplistic a task to be considered a true episodic memory task (rather it is considered a task of recognition memory), the WWWhich task is able to model episodic-like memory.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Touchscreen versions of this task are also available in which the nose poke holes and stimulus lights are replaced with an LCD screen (Romberg et al., 2011; Bussey et al., 2012).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling attention
What the sources say
- Not checked yetcites Romberg et al., 2011
- Not checked yetcites Bussey et al., 2012
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, the contributions of both background strain and likely overexpression of mutant human APP genes on brain development and function must always be considered with regard to observed cognitive deficits in the various AD mouse models.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although no one animal model fully replicates the progression of cognitive impairments seen in the human disease, AD mouse models have been invaluable in advancing our knowledge of the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Deficits in recognition memory appear to develop after the working memory deficits in this model, as the first reported deficits in the NOR task are at 6 months old (Dodart et al., 1999).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > PDAPP
What the sources say
- Not checked yetcites Dodart et al., 1999
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Each transgenic mouse model of AD provides different insights into aspects of AD pathogenesis and the cognitive deficits associated with the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“TgCRND8 are impaired on spatial working memory tasks starting at 3 months of age. These deficits are seen in the MWM and progress with age of the animal (Janus et al., 2000; Chishti et al., 2001; Gortz et al., 2008; Richter et al., 2008; Ambree et al., 2009).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > TgCRND8
What the sources say
- Not checked yetcites Janus et al., 2000
- Not checked yetcites Chishti et al., 2001
- Not checked yetcites Gortz et al., 2008
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The deficits appear to be progressive with age, and at 12 months old the animals also show cognitive deficits in a reference memory version of the Barnes maze (Prut et al., 2007).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP23
What the sources say
- Not checked yetcites Prut et al., 2007
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The cognitive deficits in recognition memory do not appear as robust as those in working memory in this model as there are inconsistent reports in the literature (Dodart et al., 1999, 2002; Chen et al., 2000).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > PDAPP
What the sources say
- Not checked yetcites Dodart et al., 1999, 2002
- Not checked yetcites Chen et al., 2000
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“It should be noted that most of the AD mouse models are representative of the familial form of AD (FAD) which accounts for only a small percentage of the total AD cases each year (Campion et al., 1999).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
What the sources say
- Not checked yetcites Campion et al., 1999
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Impairments in reference memory develop by 6 months and persist through the rest of the life of this model (Reiserer et al., 2007; Bernardo et al., 2009; O'leary and Brown, 2009).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP/PS1
What the sources say
- Not checked yetcites Reiserer et al., 2007
- Not checked yetcites Bernardo et al., 2009 source
- Not checked yetcites O'leary and Brown, 2009
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Cognitive deficits are first seen at 3 months of age in the RAWM spatial working memory task and are also reported by 6 months of age in the MWM (Cao et al., 2007; Ding et al., 2008).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP/PS1
What the sources say
- Not checked yetcites Cao et al., 2007
- Not checked yetcites Ding et al., 2008
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“However, they do not appear to progress with the age of the animal and there has even been a report of no recognition memory deficits in old animals in advanced stages of the disease (Karl et al., 2012).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > J20
What the sources say
- Not checked yetcites Karl et al., 2012
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These working memory deficits are followed temporally with the development of associative learning impairment in fear conditioning (Ohno et al., 2006; Devi and Ohno, 2010) as well as the development of deficits in a working memory version of the Y-maze (Oakley et al., 2006; Devi and Ohno, 2012; Shukla et al., 2013).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > 5×FAD
What the sources say
- Not checked yetcites Ohno et al., 2006
- Not checked yetcites Devi and Ohno, 2010
- Not checked yetcites Oakley et al., 2006
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The APP/PS1 knock-in mouse model (first described in Flood et al., 2002) uses endogenous promoters to drive the expression of humanized amyloid beta sequence, and AD-like pathology and cognitive deficits develop in the absence of APP or PS1 overexpression (Flood et al., 2002).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP/PS1 KI
What the sources say
- Not checked yetcites Flood et al., 2002
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The first observable deficits in this model are shown in associative learning and present themselves between 4 and 5 months of age (Dineley et al., 2002).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP + PS1
What the sources say
- Not checked yetcites Dineley et al., 2002
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These deficits are followed by impairments in associative memory (appearing by 14 months of age Thibault et al., 2012) and in recognition memory (not developing until 15 months of age Webster et al., 2013).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP/PS1 KI
What the sources say
- Not checked yetcites Thibault et al., 2012
- Not checked yetcites Webster et al., 2013
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Indeed, these non-cognitive symptoms are seen as a very important concern among the family members of the patients and caregivers alike (Tan et al., 2005).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models
What the sources say
- Not checked yetcites Tan et al., 2005
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Further, these disturbances increase with the age of the animals and with the severity of the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Locomotor activity
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These non-cognitive symptoms are often more difficult to deal with, as they compose important sources of distress and psychological burden on the family members/caregivers and can drastically affect the quality of life of patients by leading to institutionalization (Hope et al., 1998; Shin et al., 2005).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models
What the sources say
- Not checked yetcites Hope et al., 1998
- Not checked yetcites Shin et al., 2005
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“This suggests that perhaps aggressive deficits correlate best with moderate to severe stages of the disease, which is also what is observed clinically in human AD”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Senanarong et al., 2004
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Numerous meta-analysis studies have linked depression and AD”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Depressive symptoms
What the sources say
- Not checked yetcites Chen et al., 1999
- Not checked yetcites Charlson and Peterson, 2002
- Not checked yetcites Ownby et al., 2006
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“These disturbances are characterized by the AD patient's propensity to frequently awaken during the nighttime and to increase the amount of time slept during the day”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Circadian rhythm and sleep disruptions
What the sources say
- Not checked yetcites Ancoli-Israel et al., 1989 source
- Not checked yetcites Okawa et al., 1991
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“AD is not just a memory disorder, rather it is a complex disease with many different non-cognitive neuropsychiatric symptoms which are an important source of distress and a psychological burden on family members and caregivers alike.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Conclusions
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“No one animal model fully replicates the pathogenesis of AD, but rather only model different aspects of the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Conclusions
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the anatomical makeup and cognitive ability of mice make it difficult to model all of the intricacies of higher-order cognitive function exclusive to humans.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Conclusions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper relies on this without support.
No animal model recapitulates the entirety of AD in humans.
“However, no animal model recapitulates the entirety of AD in humans, and therefore it is important to understand both the utility and limitations of particular animal models.”
The paper relies on this without support.
Outside of frontotemporal lobar degeneration (FTLD), one does not see widespread cortical NFTs without abundant plaque pathology.
“It should be noted that outside of frontotemporal lobar degeneration (FTLD), one does not see widespread cortical NFTs without abundant plaque pathology.”
The paper relies on this without support.
During late stages (Braak stage V–VI), NFTs increase in number and manifest in neocortical areas responsible for higher cognitive domains such as executive function, visuospatial capacities, and speech in synchrony with observed AD-related cognitive deficits in these respective cognitive domains.
“During the late stages (Braak stage V–VI), NFTs increase in number and manifest in neocortical areas responsible for higher cognitive domains such as executive function, visuospatial capacities, and speech in synchrony with observed AD-related cognitive deficits in these respective cognitive domains.”
The paper relies on this without support.
Some of the earliest neuropathological changes in AD are in the hippocampus and entorhinal cortex, followed by changes in the medial temporal lobe.
“Some of the earliest neuropathological changes in AD are in the hippocampus and entorhinal cortex, followed by changes in the medial temporal lobe.”
The paper relies on this without support.
Neuropsychological assessment is the most reliable means to clinically evaluate the cognitive deficits seen in humans.
“Neuropsychological assessment is the most reliable means to clinically evaluate the cognitive deficits seen in humans.”
The paper relies on this without support.
Other cognitive domains impaired in human AD such as those involving language (i.e., verbal acuity tasks and verbal recall tasks) simply cannot be modeled in rodent models.
“Other cognitive domains impaired in human AD such as those involving language (i.e., verbal acuity tasks and verbal recall tasks) simply cannot be modeled in rodent models.”
The paper relies on this without support.
Working memory is perhaps one of the most well modeled aspects of the memory deficits in AD.
“Working memory is perhaps one of the most well modeled aspects of the memory deficits in AD.”
The paper relies on this without support.
As the patient moves from the preclinical phase of AD into MCI, more cognitive domains begin to be affected.
“As the patient moves from the preclinical phase of AD into MCI, more cognitive domains begin to be affected.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In preclinical AD, mouse models that contain a mutation in amyloid precursor protein (APP) have been widely used as models of AD, which play an essential role in cognitive function (Webster et al., 2014).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Webster et al., 2014
Experimental — accuracy not yet measuredIn the citing paper
“There have been many clinicopathological studies that have correlated amyloid plaques with cognitive deficits in AD, with an emerging picture that the strongest correlation exists in the earliest stages of the disease and this association greatly weakens as NFTs and neocortical degeneration become more widespread [9, 102, 103, 157, 160, 169].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [169]
In the citing paper
“On the other hand, numerous studies have documented a strong link between neocortical NFTs and cognitive loss[26, 46, 48, 97, 123, 160, 169].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [169]
Citations
Cites
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The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment
Nasreddine, Z. S., Phillips, N. A., Bédirian, V., Charbonneau, S., Whitehead, V., Collin, I., Cummings, J. L., & Chertkow, H. (2005) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.2005.53221.x · Cited by 25,553
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657 · cited 1×
“Once the AD patient progresses past MCI and into dementia, general cognition continues to decline with deficits appearing in all respective cognitive domains (Huff et al., 1987; Locascio et al., 1995; Lambon Ralph et al., 2003; Mckhann et al., 2011).”
BackgroundPlace navigation impaired in rats with hippocampal lesions
Morris, R. G. M., Garrud, P., Rawlins, J. N. P., & O'Keefe, J. (1982) · Nature · doi:10.1038/297681a0 · Cited by 6,340 · cited 8×
“In this model, the cognitive deficits first present themselves in spatial working memory at 4 months of age when assessed by MWM testing (Hartman et al., 2005).”
MethodInfluentialKaplan, E., Goodglass, H., Weıntraub, S., & Segal, O. (2001) · Medical Entomology and Zoology · Cited by 4,378
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210 · cited 6×
“(Promoter: Hamster PrP Promoter, Symbol: Tg (APPSWE) 2576Kha, MGI ID: 2385631) In the Tg2576 mouse (Hsiao et al., 1996), the first presentation of cognitive deficits is seen at 5 months of age in spatial working memory (Arendash et al., 2004).”
BackgroundMethodInfluentialA new rating scale for Alzheimer's disease
(1984) · American Journal of Psychiatry · doi:10.1176/ajp.141.11.1356 · Cited by 4,175 · cited 1×
“The Alzheimer’s Disease Assessment Scale (ADAS) was specifically developed to measure the severity of symptoms commonly seen in AD (Rosen et al., 1984).”
MethodMoms, J. C., Heyman, A., Mohs, R. C., Hughes, J. P., van Belle, G., Fillenbaum, G., Mellits, E. D., & Clark, C. (1989) · Neurology · doi:10.1212/wnl.39.9.1159 · Cited by 4,130 · cited 1×
“…tests are extensively used as clinical diagnostic tools (Schmitt, 1994) as well as to track the progression of the disease (Flicker et al., 1984; Morris et al., 1989; Storandt and Hill, 1989; Storandt, 1991; Welsh et al., 1991, 1992; Locascio et al., 1995; Albert, 1996; Storandt et al., 1998;…”
MethodTriple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126 · cited 1×
“…2006), 25: (Ohno et al., 2006), 26: (Shukla et al., 2013), 27: (Devi and Ohno, 2010), 28:(Devi and Ohno, 2012), 29: (Urano and Tohda, 2010), 30: (Oddo et al., 2003), 31: (Clinton et al., 2007), 32: (Carroll et al., 2007), 33: (Gimenez-Llort et al., 2007), 34: (Billings et al., 2005), 35:…”
Blessed, G., Tomlinson, B. E., & Roth, M. (1968) · British Journal of Psychiatry · doi:10.1192/bjp.114.512.797 · Cited by 4,117 · cited 1×
“There have been numerous clinicopathological studies attempting to correlate amyloid plaques with the cognitive deficits seen in AD (Blessed et al., 1968; Tomlinson et al., 1970; Duyckaerts et al., 1990, 1998; Berg et al., 1998; Gold et al., 2000; Mungas et al., 2001; Tiraboschi et al., 2002, 2004;…”
Background
Flagged first, then by citations
Research works printed but not linked: 2
- Benedict, 1994, Preliminary standardization and validation of a multiple-form test for the assessment of visuospatial memory, Arch. Clin. Neuropsychol, 9, 109
- Benton, 1992, Benton Visual Retention Test, 5th Edn
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Items 101–200 of 752
Emotional and cognitive changes in chronic kidney disease
Kim, D., Kim, S.-W., & Gil, H. (2022) · The Korean Journal of Internal Medicine · doi:10.3904/kjim.2021.492 · Cited by 70
“Barnes maze Rat, Mouse Spatial learning and memory Decreased contextual fear memory in dementia and Alzheimer’s disease [40,41] Requires multiple days of training”
BackgroundMethodLong, Q., Li, T., Zhu, Q., He, L., & Zhao, B.-B. (2023) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2023.117679 · Cited by 67
Sun, X.-H., Dong, Y.-X., Zhang, H.-Y., Li, H.-Y., Liu, P.-H., & Sui, Y. (2018) · Neural Regeneration Research · doi:10.4103/1673-5374.232486 · Cited by 67
“Although cognitive deficits in APP/PS1 mice have also been seen the spatial working memory in radial arm water maze task as early as 3 months (Webster et al., 2014), the present study failed to find spatial memory and learning impairments in 3-month-old APP/PS1 mice.”
BackgroundYamamoto, S., Kayama, T., Noguchi‐Shinohara, M., Hamaguchi, T., Yamada, M., Abe, K., & Kobayashi, S. (2021) · npj Science of Food · doi:10.1038/s41538-021-00084-5 · Cited by 69
Chen, Y., Chen, X., Luo, Z., Kang, X., Ge, Y., Wan, R., Wang, Q., Han, Z., Li, F., Fan, Z., et al. (2024) · Journal of Advanced Research · doi:10.1016/j.jare.2024.03.025 · Cited by 67
“It is critical to recognize that these models may not entirely capture the complexity of AD in humans, and that establishing causality necessitates further study [89–91].”
Rizzo, S. J. S., & Crawley, J. N. (2017) · Annual Review of Animal Biosciences · doi:10.1146/annurev-animal-022516-022754 · Cited by 67
Li, X., Men, W., Zhu, H., Lei, J., Zuo, F., Wang, Z., Zhu, Z., Bao, X., & Wang, R. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17101707 · Cited by 66
“Thus, based on our and previous findings [13,15], Tg mice of four ages used in this study mimicked the pre-, sub-, early- and mid-clinical stage of AD.”
BackgroundTracking progressive pathological and functional decline in the rTg4510 mouse model of tauopathy
Blackmore, T., Meftah, S., Murray, T. K., Craig, P. J., Blockeel, A., Phillips, K., Eastwood, B., O’Neill, M. J., Marston, H., Ahmed, Z., et al. (2017) · Alzheimer's Research & Therapy · doi:10.1186/s13195-017-0306-2 · Cited by 66
Sakakibara, Y., Sekiya, M., Saito, T., Saido, T. C., & Iijima, K. M. (2019) · BMC Neuroscience · doi:10.1186/s12868-019-0496-6 · Cited by 65
Roy, J., Wong, K. Y., Aquili, L., Uddin, M. S., Heng, B. C., Tipoe, G. L., Wong, K.-H., Fung, M., & Lim, L. W. (2022) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2022.100986 · Cited by 64
Absence of Prenatal Forebrain Defects in the Dp(16)1Yey/+ Mouse Model of down Syndrome.
Goodliffe, J. W., Olmos-Serrano, J. L., Aziz, N. M., Pennings, J. L. A., Guedj, F., Bianchi, D. W., & Haydar, T. F. (2016) · The Journal of Neuroscience · doi:10.1523/jneurosci.2513-15.2016 · Cited by 65
“…disorders such as autism spectrum disorder (Moy et al., 2009; Brielmaier et al., 2012; Speed et al., 2015) and Alzheimer’s disease (Janus et al., 2000; Van Dam et al., 2003; Arendash et al., 2004; Hartman et al., 2005; Webster et al., 2014) despite rather dissimilar genetic underpinnings.”
BackgroundSex Differences in Healthspan Predict Lifespan in the 3xTg-AD Mouse Model of Alzheimer’s Disease
Kane, A. E., Shin, S., Wong, A. A., Fertan, E., Faustova, N. S., Howlett, S. E., & Brown, R. E. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00172 · Cited by 65
“, 2017), the 3xTg-AD mouse has been considered one of the most important models of AD as it develops both plaques and tangles (Webster et al., 2014; Esquerda-Canals et al., 2017).”
BackgroundSteroids and Alzheimer’s Disease: Changes Associated with Pathology and Therapeutic Potential
Akwa, Y. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21134812 · Cited by 66
“Although animal AD models do not fully recapitulate human AD cognitive deficits, they are a very useful tool for assessing memory functioning and pharmacological intervention in behavioral tasks [153].”
BackgroundThe two faces of synaptic failure in AppNL-G-F knock-in mice
Latif‐Hernandez, A., Sabanov, V., Ahmed, T., Craessaerts, K., Saito, T., Saido, T. C., & Balschun, D. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00667-6 · Cited by 68
“network, and behavioral levels is important to understand the utility and limitations of each model [50].”
BackgroundAnimal Models in Translational Research: Rosetta Stone or Stumbling Block?
Bolker, J. A. (2017) · BioEssays · doi:10.1002/bies.201700089 · Cited by 68
Li, S., Jin, M., Liu, L., Dang, Y., Ostaszewski, B. L., & Selkoe, D. J. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0626-x · Cited by 64
“mice, spatial learning and memory have been shown to be impaired in nearly all models of Aβ overproduction by transgenic APP expression, and the onset of the cognitive decline occurred close to that of brain amyloid deposition [76].”
Nackenoff, A. G., Hohman, T. J., Neuner, S. M., Akers, C. S., Weitzel, N. C., Shostak, A., Ferguson, S. M., Mobley, B., Bennett, D. A., Schneider, J. A., et al. (2021) · PLOS Genetics · doi:10.1371/journal.pgen.1009406 · Cited by 59
“While considerable protease immunoreactivity has been observed around β-amyloid plaques, lysosomes in dystrophic neurites appear to be functioning sub-optimally based on our observation that they are deficient in lysosomal proteases [35,38,49] compared to lysosomes in neuronal cell bodies (Fig 1 and Fig B in S1 Text).”
BackgroundMethodFolic acid administration inhibits amyloid β-peptide accumulation in APP/PS1 transgenic mice
Li, W., Liu, H., Yu, M., Zhang, X., Zhang, M., Wilson, J. X., & Huang, G. (2015) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2015.03.009 · Cited by 62
“not occur in the APP/PS1 mouse [21,30].”
BackgroundInfluentialHansen, H. H., Fabricius, K., Barkholt, P., Wismann, P., Schlumberger, C., Jelsing, J., Terwel, D., Termont, A., Pyke, C., Knudsen, L. B., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0158205 · Cited by 65
O’Leary, T. P., & Brown, R. E. (2022) · Genes Brain & Behavior · doi:10.1111/gbb.12794 · Cited by 61
“Among control measures that gauge sensori-motor confounds, no genotype differences were found in swim speed, but female mice swam significantly faster than males in both acquisition (F[1, 38] = 5.”
BackgroundNeutrophils as a potential therapeutic target in Alzheimer’s disease
Aries, M. L., & Hensley‐McBain, T. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1123149 · Cited by 62
“All of these models overexpress Ab in the CNS and develop diffuse Ab plaques starting as early as 2-3 months of age (19).”
BackgroundInfluentialFan, S., Xian, X., Li, L., Yao, X., Hu, Y., Zhang, M., & Li, W. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180708 · Cited by 61
“These mice show learning and memory deficits in the age of 3–5 months and plentiful senile plaques in 12 months, and manifest similar pathological characteristics with AD patients [23].”
Kamdi, S. P., Raval, A., & Nakhate, K. T. (2021) · Cytokine · doi:10.1016/j.cyto.2020.155408 · Cited by 61
Analysis of RNA from Alzheimer’s Disease Post-mortem Brain Tissues
Clement, C., Hill, J. M., Dua, P., Culicchia, F., & Lukiw, W. J. (2016) · Molecular Neurobiology · doi:10.1007/s12035-015-9105-6 · Cited by 54
Lachén‐Montes, M., González-Morales, A., de Morentin, X. M., Pérez‐Valderrama, E., Ausín, K., Zelaya, M. V., Serna, A., Aso, E., Ferrer, I., Fernández‐Irigoyen, J., et al. (2016) · Journal of Proteomics · doi:10.1016/j.jprot.2016.07.032 · Cited by 61
Long-term RF exposure on behavior and cerebral glucose metabolism in 5xFAD mice
Son, Y., Kim, J. S., Jeong, Y. J., Jeong, Y. K., Kwon, J. H., Choi, H., Pack, J., Kim, N., Lee, Y., & Lee, H. (2017) · Neuroscience Letters · doi:10.1016/j.neulet.2017.12.042 · Cited by 63
Lee, H., Jeon, S. G., Kim, J., Kang, R. J., Kim, S., Han, K., Park, H., Kim, K., Sung, Y. M., Nam, H. Y., et al. (2021) · Aging Cell · doi:10.1111/acel.13332 · Cited by 62
“…amyloid plaques, and tau phosphorylation (Figures 1– 5), we evaluated the behavioral performance of 3- month- old 5xFAD and PS19 mice injected with ibrutinib (10 mg/kg; i.p.) or vehicle daily for 14 days by conducting Y- maze and novel object recognition (NOR) tests (Webster et al., 2014).”
MethodGatta, E., Lefebvre, T., Gaetani, S., Santos, M. D., Marrocco, J., Mir, A., Cassano, T., Maccari, S., Nicoletti, F., & Mairesse, J. (2016) · Pharmacological Research · doi:10.1016/j.phrs.2016.01.006 · Cited by 62
“The reduction of O-GlcNAcylation we have found in the hippocampus of 12-month-old 3xTg-AD mice may have a deep impact on the pathological phenotype of these mice contributing to tau aggregation, synaptic dysfunction, behavioral abnormalities, and neurodegeneration (Webster et al., 2014).”
BackgroundReview: Neuropathology and behavioural features of transgenic murine models of Alzheimer's disease
Ameen‐Ali, K. E., Wharton, S. B., Simpson, J. E., Heath, P. R., Sharp, P. S., & Berwick, J. (2017) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12440 · Cited by 59
Ahmed, H. A., Ishrat, T., Pillai, B. A., Fouda, A. Y., Sayed, M. A., Eldahshan, W., Waller, J. L., Ergul, A., & Fagan, S. C. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1262-x · Cited by 59
Lia, A., Sansevero, G., Chiavegato, A., Sbrissa, M., Pendin, D., Mariotti, L., Pozzan, T., Berardi, N., Carmignoto, G., Fasolato, C., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-37240-2 · Cited by 63
Sun, Y., Rong, X., Lu, W., Peng, Y., Jiang, L., Xu, S., Wang, L., & Wang, X. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-142805 · Cited by 58
“Transgenic mice overexpressing mutant A (cid:1) PP and PS1 (A PP/PS1) have been widely used as a model and to investigate candidate biomarkers Previous studies have shown that neuropathological changes in this including increased A (cid:1) production and accelerated amyloid deposition [17].”
Zou, C., Montagna, E., Shi, Y., Peters, F., Blázquez‐Llorca, L., Shi, S., Filser, S., Dorostkar, M. M., & Herms, J. W. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1421-4 · Cited by 63
“Among the APP transgenic mouse models, APP23 and APPswe/PS1deltaE9 (deltaE9) mice have been extensively used for exploring AD-related pathology and drug development [63].”
BackgroundA second wind for the cholinergic system in Alzheimer’s therapy
Douchamps, V., & Mathis, C. (2017) · Behavioural Pharmacology · doi:10.1097/fbp.0000000000000300 · Cited by 61
“The pattern of cognitive impairment is reminiscent of the one found in AD: most models show deficits in working memory, recognition memory, spatial navigation memory, and even in the newly developed episodic-like memory tasks (Webster et al., 2014).”
ResultIntracellular Calcium Dysregulation by the Alzheimer’s Disease-Linked Protein Presenilin 2
Galla, L., Redolfi, N., Pozzan, T., Pizzo, P., & Greotti, E. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21030770 · Cited by 57
“, overproduction of APP fragments in addition to Aβ [211] and lack of a clear phenotype standardization of the different models [212].”
BackgroundHansson, O., Svensson, M., Gustavsson, A., Andersson, E., Yang, Y., Nägga, K., Hållmarker, U., James, S. K., & Deierborg, T. (2019) · Alzheimer s Research & Therapy · doi:10.1186/s13195-019-0538-4 · Cited by 60
Nirzhor, S. S. R., Khan, R. I., & Neelotpol, S. (2018) · Biomolecules · doi:10.3390/biom8030093 · Cited by 57
“In murine odels, it has been observed t at m phological change in micro lia ccurs at a igher rate i ged mice (12 months or older) compar d to oth r age g oups [31,32].”
BackgroundInfluentialKim, C. H., Romberg, C., Hvoslef‐Eide, M., Oomen, C. A., Mar, A. C., Heath, C. J., Berthiaume, A., Bussey, T. J., & Saksida, L. M. (2015) · Psychopharmacology · doi:10.1007/s00213-015-4017-8 · Cited by 58
“However, many animal models expressing diseaserelated genetic abnormalities are exclusively available in mice (Papaleo et al. 2012; Webster et al. 2014), and the TUNL task has only been available for the rat.”
BackgroundCross-species translation of the Morris maze for Alzheimer’s disease
Possin, K. L., Sanchez, P. E., Anderson-Bergman, C., Fernandez, R., Kerchner, G. A., Johnson, E. T., Davis, A., Lo, I., Bott, N. T., Kiely, T., et al. (2016) · Journal of Clinical Investigation · doi:10.1172/jci78464 · Cited by 56
“One reason is that the clinical tests used in patients minimally resemble the laboratory tests used to probe cognitive aspects of AD in animal models (5).”
BackgroundMethodVeening-Griffioen, D. H., Ferreira, G. S., van Meer, P. J. K., Boon, W., Wied, C. C. G., Moors, E. H. M., & Schellekens, H. (2019) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2019.172524 · Cited by 59
“For complex diseases such as Alzheimer's disease one could consider a (properly designed) test battery of different (animal) models simulating different aspects of the disease (Stukalin and Einat, 2019; Webster et al., 2014; Wolf et al., 2016).”
BackgroundExercise-Induced Modulation of Neuroinflammation in Models of Alzheimer’s Disease
Kelly, Á. M. (2018) · Brain Plasticity · doi:10.3233/bpl-180074 · Cited by 55
“Cognitive deficits and impaired synaptic plasticity are consistently, and sometimes simultaneously, observed in mouse models of AD, as has been reviewed several times [52, 69], however these impairments do not always correlate temporally with AD-like pathology [50].”
BackgroundOlajide, O. J., Gbadamosi, I., Yawson, E. O., Arogundade, T. T., Lewu, F. S., Ogunrinola, K. Y., Adigun, O. O., Bamisi, O., Lambe, E., Arietarhire, L. O., et al. (2021) · Journal of Molecular Neuroscience · doi:10.1007/s12031-020-01747-w · Cited by 58
“In contrast to these results, studies by Webster et al. (2014) and Whyte et al. (2018) found a significant reduction in the exploratory drive and social interaction of transgenic AD rat models, although Filali et al. (2011) also noted hyperactivity in the APPswe/PS1 mouse.”
ResultCurdt, N., Schmitt, F. W., Bouter, C., Iseni, T., Weile, H. C., Altunok, B., Beindorff, N., Bayer, T. A., Cooke, M. B., & Bouter, Y. (2022) · Scientific Reports · doi:10.1038/s41598-022-09270-1 · Cited by 63
“3G: unpaired t-test, genotype: F(10,12) = 11.”
Self-citationHan, B., Yu, L., Geng, Y., Li, S., Wang, H., Wang, Y., Wang, J., & Wang, M. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160189 · Cited by 57
“APP/PS1 double transgenic mice are a classic model of AD, which exhibit progressive cognitive impairments and neuropathological changes with age [23, 24].”
MMP13 inhibition rescues cognitive decline in Alzheimer transgenic mice via BACE1 regulation
Zhu, B., Long, Y., Luo, W., Yan, Z., Lai, Y., Zhao, L., Zhou, W., Wang, Y., Shen, L., Liu, L., et al. (2018) · Brain · doi:10.1093/brain/awy305 · Cited by 53
“To determine whether CL82198 or MMP13 may affect cognitive functions, we assessed spatial and associative learning memory using water maze tests and context fear conditioning tests in animals with Mmp13 knockdown or CL82198 treatment (Ly et al., 2013; Webster et al., 2014).”
BackgroundJew, K., Herr, D., Wong, C., Kennell, A., Morris‐Schaffer, K., Oberdörster, G., O’Banion, M. K., Cory‐Slechta, D. A., & Elder, A. C. P. (2019) · Particle and Fibre Toxicology · doi:10.1186/s12989-019-0323-3 · Cited by 55
Cassel, J., Ferraris, M., Quilichini, P., Cholvin, T., Boch, L., Stéphan, A., & de Vasconcelos, A. P. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.03.023 · Cited by 56
Poon, A., Zhang, Y., Chandrasekaran, A., Phanthong, P., Schmid, B., Nielsen, T. T., & Freude, K. (2017) · New Biotechnology · doi:10.1016/j.nbt.2017.05.009 · Cited by 54
Alzheimer's disease: Only prevention makes sense
Viña, J., & Sanz‐Ros, J. (2018) · European Journal of Clinical Investigation · doi:10.1111/eci.13005 · Cited by 55
“They usually focus on one or a few pathophysiological aspects of the disease.(40) There are obvious differences between mice and human AD.”
BackgroundHao, J.-R., Sun, N., Lei, L., Li, X.-Y., Yao, B., Sun, K., Hu, R., Zhang, X., Shi, X.-D., & Gao, C. (2015) · Cell Death & Disease · doi:10.1038/cddis.2015.315 · Cited by 53
“L-SPD may be explored as a potential therapeutic drug for AD.”
BackgroundInfluentialAge-related cognitive decline in spatial learning and memory of C57BL/6J mice
Hendrickx, J. O., Moudt, S. D., Calus, E., Deyn, P. P. D., Dam, D. V., & Meyer, G. R. Y. D. (2021) · Behavioural Brain Research · doi:10.1016/j.bbr.2021.113649 · Cited by 56
“Most frequently used behavioural assays in neurodegenerative GEM models concern testing of spatial learning and memory such as the MWM, though simple tests such as the Y-maze and T-maze are also often employed [25].”
Martín‐Sánchez, A., Piñero, J., Nonell, L., Arnal, M., Ribé, E. M., Nevado‐Holgado, A. J., Lovestone, S., Sanz, F., Furlong, L. I., & Valverde, O. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-021-00810-x · Cited by 52
Owlett, L. D., Karaahmet, B., Le, L., Belcher, E. K., Dionisio-Santos, D. A., Olschowka, J. A., Elliott, M. R., & O’Banion, M. K. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02397-y · Cited by 53
“Aged APP/PS1 mice demonstrate deficits in a number of hippocampal dependent tasks, including those that assess recognition and conditioned memory such as the novel object recognition task and the conditioned and cued fear conditioning task [32].”
BackgroundRoddick, K. M., Roberts, A. D., Schellinck, H. M., & Brown, R. E. (2016) · Chemical Senses · doi:10.1093/chemse/bjw018 · Cited by 51
“2013, 2014) and 3xTg-AD mice (Webster et al. 2014), we tested our mice at 6 months of age.”
BackgroundMethodHan, B., Wang, J., Geng, Y., Shen, L., Wang, H.-L., Wang, Y.-Y., & Wang, M. (2017) · Cellular Physiology and Biochemistry · doi:10.1159/000471869 · Cited by 52
Estrogen-related receptor alpha is involved in Alzheimer's disease-like pathology
Tang, Y., Min, Z., Xiang, X., Liu, L., Ma, Y., Zhu, B., Li, S., Tang, J., Deng, X., Yan, Z., et al. (2018) · Experimental Neurology · doi:10.1016/j.expneurol.2018.04.003 · Cited by 51
“6–8weeks in both cortex and hippocampus, which exists throughout life span (Bilkei-Gorzo, 2014; Webster et al., 2014).”
Wu, S., Liu, H., Zhao, H., Wang, X., Chen, J., Xia, D., Chen, X., Cheng, J., Zhao, Z., & He, Y. (2019) · Toxicology Letters · doi:10.1016/j.toxlet.2019.11.009 · Cited by 51
Rajamohamedsait, H., Rasool, S., Rajamohamedsait, W., Lin, Y., & Sigurdsson, E. M. (2017) · Scientific Reports · doi:10.1038/s41598-017-17313-1 · Cited by 49
Songvut, P., Chariyavilaskul, P., Tantisira, M. H., & Khemawoot, P. (2019) · Planta Medica · doi:10.1055/a-0835-6671 · Cited by 50
“As the accumulation of beta-amyloid is considered a hallmark of Alzheimerʼs disease, approaches dealing with amyloid have been proposed to slow disease progression [3].”
BackgroundEarly Cognitive and Behavioral Deficits in Mouse Models for Tauopathy and Alzheimer’s Disease
Samaey, C., Schreurs, A., Stroobants, S., & Balschun, D. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00335 · Cited by 57
“As a consequence, different animal models have been introduced for different research questions (Webster et al., 2014).”
BackgroundInfluentialSharma, M., Pal, P., & Gupta, S. K. (2024) · Neurochemistry International · doi:10.1016/j.neuint.2024.105761 · Cited by 49
Myostatin Is Associated With Cognitive Decline in an Animal Model of Alzheimer’s Disease
Lin, Y.-S., Lin, F.-Y., & Hsiao, Y. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1201-y · Cited by 48
McAllister, B. B., Lacoursiere, S. G., Sutherland, R. J., & Mohajerani, M. H. (2020) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2020.01.026 · Cited by 48
Bray, E. E., Raichlen, D. A., Forsyth, K. K., Promislow, D., Alexander, G. E., MacLean, E. L., Akey, J. M., Benton, B., Borenstein, E., Castelhano, M. G., et al. (2022) · GeroScience · doi:10.1007/s11357-022-00655-8 · Cited by 47
“However, these models have typically focused on the least prevalent form in humans [17].”
BackgroundPreclinical models in the study of sex differences
Buoncervello, M., Marconi, M., Carè, A., Piscopo, P., Malorni, W., & Matarrese, P. (2017) · Clinical Science · doi:10.1042/cs20160847 · Cited by 47
Unger, M. S., Marschallinger, J., Kaindl, J., Klein, B., Johnson, M. A., Khundakar, A. A., Roßner, S., Heneka, M. T., Couillard‐Després, S., Rockenstein, E. M., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.02.017 · Cited by 48
“These changes in brain structure and function lead to a decline in cognitive performance of these mice, tested in several cognitive behavior tasks [55,57].”
Goto, T., Kuramoto, E., Dhar, A., Wang, R. P., Seki, H., Iwai, H., Yamanaka, A., Matsumoto, S., Hara, H., Michikawa, M., et al. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200257 · Cited by 48
Hascup, K. N., & Hascup, E. R. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-142160 · Cited by 49
“We did not observe differences between genotypes during training or probe in any of the parameters measured (data not shown) as reported elsewhere [35].”
8-Hydroxyquinolylnitrones as multifunctional ligands for the therapy of neurodegenerative diseases
Knez, D., Diez‐Iriepa, D., Chioua, M., Gottinger, A., Denic, M., Chantegreil, F., Nachon, F., Brazzolotto, X., Skrzypczak-Wiercioch, A., Meden, A., et al. (2023) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2023.01.013 · Cited by 46
Alzheimer’s Disease Model System Using Drosophila
Tsuda, L., & Lim, Y. (2018) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-0529-0_3 · Cited by 48
Roda, A. R., Esquerda-Canals, G., Martı́, J., & Villegas, S. (2020) · Pharmaceutics · doi:10.3390/pharmaceutics12100944 · Cited by 47
“Associative learning deficits are first detected at around 3–5 months of age, impairments in spatial working memory in the Morris water maze (MWM) paradigm at 6 months, deficits in recognition memory at around 9–11 months, and reference memory impairment in the Barnes maze task at 12 months [19].”
BackgroundAlzheimer’s Disease: From Immune Homeostasis to Neuroinflammatory Condition
Cariddi, L. P., Mauri, M. F., Cosentino, M., Versino, M., & Marino, F. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232113008 · Cited by 45
“I EOAD atients, these pathological findings could be fully expl ined by th mutations det cted in different genes involved in APP synthesis and metab lism (APP, PS1 and/or PS2 gen s) [15,16], and suppo ted by the f ndings in transgenic mice, expressing at least one of thes human mutated genes, that showed the same pecu…”
BackgroundJiang, J., Pan, H., Shen, F., Tan, Y., & Chen, S. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.373715 · Cited by 50
Perentos, N., Martins, A. Q., Watson, T. C., Bartsch, U., Mitchell, N. L., Palmer, D. N., Jones, M. W., & Morton, A. J. (2015) · Brain · doi:10.1093/brain/awv026 · Cited by 49
“the relevant pathology or doing so at such a late stage in their lives that they cannot be used effectively (LaFerla and Green, 2012; Pouladi et al., 2013; Webster et al., 2014).”
BackgroundEvgen’ev, M. B., Krasnov, G. S., Nesterova, I. V., Garbuz, D. G., Карпов, В. Л., Morozov, A. V., Snezhkina, A. V., Samokhin, A. N., Sergeev, A., Куликов, А. М., et al. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170398 · Cited by 45
“Previously,weperformedadetailed analysisofthemajoralterationsinthestateandmor-phologyofneuronslocatedinthehippocampusand cortexofOBXmicewhichrepresentamodelofspo-radicAD[5,27,28].”
InfluentialBrunetti, D., Bottani, E., Segala, A., Marchet, S., Rossi, F., Orlando, F., Malavolta, M., Carruba, M. O., Lamperti, C., Provinciali, M., et al. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.01171 · Cited by 43
Tong, J., Zhang, J., Hao, M., Yang, J., Han, Y., Liu, X., Shi, H., Wu, M., Liu, Q.-S., & Qi, J. (2015) · Hormones and Behavior · doi:10.1016/j.yhbeh.2015.06.013 · Cited by 44
Inestrosa, N. C., Ríos, J. A., Cisternas, P., Tapia‐Rojas, C., Rivera, D. S., Braidy, N., Zolezzi, J. M., Godoy, J. A., Carvajal, F. J., Ardiles, Á. O., et al. (2014) · Brain Pathology · doi:10.1111/bpa.12226 · Cited by 47
“However, these models do not recapitulate the entire spectrum of lesions present in human AD brains (17, 42, 84).”
BackgroundTherapeutic Targeting of Casein Kinase 1δ/ε in an Alzheimer’s Disease Mouse Model
Adler, P., Mayne, J., Walker, K., Ning, Z., & Figeys, D. (2019) · Journal of Proteome Research · doi:10.1021/acs.jproteome.9b00312 · Cited by 45
Depression and Anxiety in the Epilepsies: from Bench to Bedside
Krishnan, V. (2020) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-020-01065-z · Cited by 48
Cai, H.-Y., Wang, Z., Hölscher, C., Li, Y., Zhang, J., Sun, P., Li, J., Yang, W., Wu, M., & Qi, J. (2016) · Behavioural Brain Research · doi:10.1016/j.bbr.2016.10.033 · Cited by 46
García, Y., & Esquivel, N. (2018) · Behavioral Sciences · doi:10.3390/bs8010014 · Cited by 45
“Behavioral tasks to evaluate cognitive function in laboratory animals are tools with a key role during the development of pharmaceutical formulations aimed to the treatment of neurodegenerative diseases [2,5,6].”
MethodZhu, Y., Xiong, Y., Luo, F., & Jia, M. (2018) · Neuropathology · doi:10.1111/neup.12530 · Cited by 43
Binyamin, O., Nitzan, K., Frid, K., Ungar, Y., Rosenmann, H., & Gabizon, R. (2019) · Scientific Reports · doi:10.1038/s41598-019-54971-9 · Cited by 43
Riluzole attenuates glutamatergic tone and cognitive decline in AβPP/PS1 mice
Hascup, K. N., Findley, C. A., Britz, J., Esperant‐Hilaire, N., Broderick, S. O., Delfino, K. R., Tischkau, S. A., Bartke, A., & Hascup, E. R. (2020) · Journal of Neurochemistry · doi:10.1111/jnc.15224 · Cited by 41
“In this study, AβPP/PS1 mice were treated with riluzole (2–6 months of age) prior to the onset of cognitive deficits (Minkeviciene et al., 2008; Webster et al., 2014).”
MethodShal, B., Khan, A., Khan, A. U., Ullah, R., Ali, G., Islam, S. U., Haq, I. U., Ali, H., Seo, E. K., & Khan, S. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126603 · Cited by 42
“Although none of the models completely represents the phenotypes present in AD patients, however, similar changes can be observed related to the disease progression and cognitive decline [22].”
Dissecting Alzheimer disease in Down syndrome using mouse models
Choong, X. Y., Tosh, J., Pulford, L. J., & Fisher, E. (2015) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2015.00268 · Cited by 41
“…is through studying mouse models, and a large number of transgenic strains have been generated to understand specific aspects of AD pathology, most of which have human gene mutations that give rise to rare early-onset familial Alzheimer disease (FAD; Braidy et al., 2012;Webster et al., 2014).”
BackgroundOlmos-Serrano, J. L., Tyler, W. A., Cabral, H., & Haydar, T. F. (2016) · Experimental Neurology · doi:10.1016/j.expneurol.2016.02.005 · Cited by 41
“The current findings of impairments in nesting behavior, spontaneous alternation and reversal learning are also consistent with findings in mouse models of AD (Filali and Lalonde, 2009; Morales-Corraliza et al., 2013; Torres-Lista and Gimenez-Llort, 2013; Webster et al., 2014; Devi et al., 2015).”
ResultShepherd, A. L., Tyebji, S., Hannan, A. J., & Burrows, E. L. (2016) · Journal of Molecular Neuroscience · doi:10.1007/s12031-016-0837-1 · Cited by 43
Lardenoije, R., van den Hove, D., Havermans, M., van Casteren, A., Le, K. X., Palmour, R., Lemere, C. A., & Rutten, B. P. F. (2017) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2017.11.002 · Cited by 42
“…model is widely used and cognitive impairments have been reported for spatial working memory as early as 4 months of age, with additional impairments in reference memory, associative learning, and passive avoidance with increasing age (Frost et al., 2015; Park et al., 2006; Webster et al., 2014).”
BackgroundMethodInfluentialMotor deficits in 16-month-old male and female 3xTg-AD mice
Montbrun, T. G.-D., Fertan, E., Stover, K. R., & Brown, R. E. (2018) · Behavioural Brain Research · doi:10.1016/j.bbr.2018.09.006 · Cited by 45
Impaired Spatial Reorientation in the 3xTg-AD Mouse Model of Alzheimer’s Disease
Stimmell, A. C., Baglietto‐Vargas, D., Moseley, S. C., Lapointe, V., Thompson, L. M., LaFerla, F. M., McNaughton, B. L., & Wilber, A. A. (2019) · Scientific Reports · doi:10.1038/s41598-018-37151-z · Cited by 42
Corsetti, V., Borreca, A., Latina, V., Giacovazzo, G., Pignataro, A., Krashia, P., Natale, F., Cocco, S., Rinaudo, M., Malerba, F., et al. (2020) · Brain Communications · doi:10.1093/braincomms/fcaa039 · Cited by 42
“…neuropathology could be restricted within strain-specific temporal window(s) because of the complex and multifactorial feature of Alzheimer’s disease pathology involving a wide range of inflammatory, oxidative, neurodegenerative causative mechanisms (Webster et al. , 2014; Velazquez et al. , 2018).”
Maliszewska‐Cyna, E., Xhima, K., & Aubert, I. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150660 · Cited by 41
“However, in mice with AD pathology, impairments in spatial working memory are generally the first to be observed and they are also the best studied and modeled [25].”
Loss of presenilin function is associated with a selective gain of APP function
Deyts, C., Clutter, M., Herrera, S., Jovanovic, N., GODDI, A. A., & Parent, A. (2016) · eLife · doi:10.7554/elife.15645 · Cited by 41
“…plasticity is enhanced in several mouse models expressing FADlinked PS1 variants (Parent et al., 1999; Parent and Thinakaran, 2010), which is consistent with an increase in CREB signaling, a number of these mice performed poorly in a variety of memory tasks (Webster et al., 2014; Xia et al., 2015).”
Ahmed, H. A., Ishrat, T., Pillai, B. A., Bunting, K. M., Patel, A., Vazdarjanova, A. I., Waller, J. L., Arbab, A. S., Ergul, A., & Fagan, S. C. (2017) · Behavioural Brain Research · doi:10.1016/j.bbr.2017.12.007 · Cited by 43
“During IA, the animal must actively inhibit the desire and withhold the response, to re-enter a dark chamber or explore a novel compartment, after it has experienced an aversive stimulus in that location [26].”
Panagaki, T., Gengler, S., & Hölscher, C. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180584 · Cited by 42
“As such, these mice manifest spatial acquisition and reference memory impair-mentsintheMorriswater-mazetaskattheearliesttest ageof7months,whichpersistovertherestofthelife ofthismurinemodel[66,67].”
Mitochondrial dysfunction in neurodegenerative diseases: A focus on iPSC-derived neuronal models
Trombetta-Lima, M., Sabogal-Guáqueta, A. M., & Dolga, A. M. (2021) · Cell Calcium · doi:10.1016/j.ceca.2021.102362 · Cited by 42
“Nonetheless, there is no animal model that fully covers the complexity of the disease (extensively reviewed in [55 – 57]).”
BackgroundHuang, Y., Huang, X., Zhang, L., Han, F., Pang, K., Li, X., & Shen, J. (2017) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.12775 · Cited by 39
Higham, J. P., Malik, B. R., Buhl, E., Dawson, J., Ogier, A. S., Lunnon, K., & Hodge, J. J. L. (2019) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2019.00260 · Cited by 40
Metadata
- Authors
- Webster, S. J., Bachstetter, A. D., Nelson, P. T., Schmitt, F. A., & Van Eldik, L. J.
- Affiliations
- University of Kentucky (US)
- Venue
- Frontiers in Genetics
- Publisher
- Frontiers Media SA
- Published
- 2014-04-23
- Volume
- 5
- Pages
- 88-88
- ISSN
- 1664-8021 (ISSN-L)
- PMC
- PMC4005958
- OpenAlex
- W1982313782
- Semantic Scholar
- 6bbaedb9f24f173e0fcdb0d6b5b0bfe9eb3f4679
- Cited by
- 755
- References
- 365
- Citations by year
- 2026: 36 · 2025: 51 · 2024: 60 · 2023: 72 · 2022: 64 · 2021: 57 · 2020: 63 · 2019: 63 · 2018: 79 · 2017: 71 · 2016: 76 · 2015: 48 · 2014: 14
- FWCI
- 8.15
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Genetics (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Institute on Aging (P30AG028383)
- National Institute of Nursing Research
- National Institute of Child Health and Human Development
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- Alzheimer's disease, mouse models of Alzheimer's disease, amyloid precursor protein mutations, APP/PS1 mice, PDAPP mice, Tg2576 mice, APP23 mice, TgCRND8 mice, 5xFAD mice, 3xTg-AD mice, behavioral tests, cognitive impairment, spatial memory, recognition memory, associative learning, attention, set-shifting, reversal learning, neuropsychological assessment
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