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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
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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 401–500 of 752
Yeşiltepe, M., Çimen, B., & Sara, Y. (2022) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2022.175179 · Cited by 16
Walter, K. R., Ricketts, D. K., Presswood, B. H., Smith, S. M., & Mooney, S. M. (2022) · The American Journal of Drug and Alcohol Abuse · doi:10.1080/00952990.2022.2119571 · Cited by 17
“over short time periods) are seen at 6-8mo, whereas deficits in recognition memory (the ability to remember a previously encountered stimulus or situation) emerge around 9-11mo (50).”
BackgroundCognitive-enhancing effects of hydrolysate of polygalasaponin in SAMP8 mice
Xu, P., Xu, S., Wang, K., Lü, C., Zhang, H., Pan, R., Chang, Q., Yang, Y., Li, Y., & Liu, X. (2016) · Journal of Zhejiang University SCIENCE B · doi:10.1631/jzus.b1500321 · Cited by 14
“The sporadic AD model used in drug research should not only show the cognitive deficits over specific time courses, but also imitate the pathological mechanisms underlying neuronal function (Webster et al., 2014).”
Yimam, M., Burnett, B. P., Brownell, L. A., & Jia, Q. (2016) · Behavioural Neurology · doi:10.1155/2016/7240802 · Cited by 14
“The animals were first assessed in the radial arm water maze (RAWM) task prior to being placed on the experimental diet [29, 30].”
MethodRodent Models for Alzheimer’s Disease in Drug Discovery
Barrett, J. E., & McGonigle, P. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-802810-0.00012-x · Cited by 15
Wang, X., Tao, S., Cong, P., Wang, Y., Xu, J., & Xue, C. (2017) · Journal of Functional Foods · doi:10.1016/j.jff.2017.03.030 · Cited by 14
Yang, E.-J., Mahmood, U., Kim, H.-J., Choi, M., Choi, Y., Lee, J.-P., Chang, M., & Kim, H.-S. (2017) · Journal of Pharmacological Sciences · doi:10.1016/j.jphs.2017.03.005 · Cited by 14
Hutton, C. P., Lemon, J. A., Šakić, B., Rollo, C. D., Boreham, D. R., Fahnestock, M. L., Wojtowicz, J. M., & Becker, S. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170921 · Cited by 15
“This model was chosen as one of the few to exhibit both amyloid and tau pathology concomitant with impaired memory and altered mood-related behaviors [62, 63].”
Gant, J. C., Kadish, I., Chen, K.-C., Thibault, O., Blalock, E. M., Porter, N. M., & Landfield, P. W. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180618 · Cited by 14
“Idiopathic AD does not occur in non-human species [1, 2], precluding mechanistic studies of NFT pathogenesis in normally aging animals.”
BackgroundStudy on myelin injury of AD mice treated with Shenzhiling oral liquid in the PI3K/Akt–mTOR pathway
Wang, Y., Chen, F., Wang, P., Mana, L., Sheng, N., & Huang, S. (2020) · International Journal of Immunopathology and Pharmacology · doi:10.1177/2058738420923907 · Cited by 14
BACE1 SUMOylation deregulates phosphorylation and ubiquitination in Alzheimer's disease pathology
Zhao, Y., Zhou, H., Zhao, Y., Liang, Z., Gong, X., Yu, J., Huang, T., Yang, C., Wu, M., Xiao, Y., et al. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.15870 · Cited by 13
“Data show mean ± SEM, n = 5 (c, d) cell culture preparations, unpaired t- test, two- tailed, (c) p = 0.0202, t = 2.889, df = 8; (d) p = 0.0236, t = 2.788, df = 8. at 3- month- age and amyloid plaques have emerged at 6- month- age (Webster et al., 2014).”
BackgroundInfluentialCao, Q., Kumar, M., Frazier, A., Williams, J. B., Zhao, S., & Yan, Z. (2023) · Aging · doi:10.18632/aging.205057 · Cited by 12
“In agreement with this, spatial memory deficits by Morris Water maze were found to be the earliest phenotype in AD models [46], while recognition deficits manifested later [47], similar to the symptomatic progression of AD patients.”
Hayashi, K., Hasegawa, Y., Takemoto, Y., Cao, C., Mukasa, A., & Kim‐Mitsuyama, S. (2019) · European Journal of Neuroscience · doi:10.1111/ejn.14596 · Cited by 13
den Broeck, L. V., Sierksma, A. S. R., Hansquine, P., Thonnard, D., Callaerts‐Vegh, Z., & D’Hooge, R. (2020) · Genes Brain & Behavior · doi:10.1111/gbb.12695 · Cited by 14
Gene Expression Analysis of the Endocannabinoid System in Presymptomatic APP/PS1 Mice
Vidal-Palencia, L., Ramon‐Duaso, C., González-Parra, J. A., & Busquets-García, A. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.864591 · Cited by 16
“First, we evaluated behavioral and molecular alterations at early stages, confirming that this is a period with mild behavioral impairments and absence of other neuropathological alterations according to previous literature (Bilkei-Gorzo, 2014; Webster et al., 2014; Jankowsky and Zheng, 2017; Kosel et al., 2020; Peng…”
MethodInsulin and disorders of behavioural flexibility
Sullivan, M., Fernández‐Aranda, F., Camacho‐Barcia, L., Harkin, A., Macrì, S., Mora‐Maltas, B., Jiménez‐Múrcia, S., O’Leary, A., Ottomana, A. M., Presta, M., et al. (2023) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2023.105169 · Cited by 15
“However, several AD animal models have been shown to have deficits in set-shifting and reversal learning tasks, mostly in aged animals (108, 115, 238, 239, 265), reviewed in (326).”
BackgroundMammalian Models in Alzheimer’s Research: An Update
Sharma, H., Chang, K., Hulme, J., & An, S. S. A. (2023) · Cells · doi:10.3390/cells12202459 · Cited by 12
“Differences in promoters, transgene constructs and mouse strains makes it difficult to standardize the phenotypes of different models [164,165].”
BackgroundKing, J. L., Wong, A. A., & Brown, R. E. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170805 · Cited by 13
“MousemodelsofADareengineeredtoexpress mutanthumanADgenesforamyloidprecursorpro-tein(APP),and/orthepresenilins(PS1andPS2), and/ortau[29–34].”
Mega-Analysis of Gene Expression in Mouse Models of Alzheimer’s Disease
Zhuang, B. C., Mancarci, B. O., Toker, L., & Pavlidis, P. (2019) · eNeuro · doi:10.1523/eneuro.0226-19.2019 · Cited by 14
“Despite the differences in mechanisms, many of these animal models show similar age-dependent progression in decline of cognitive functions that are similar to AD symptoms observed in human (Webster et al., 2014).”
BackgroundResultInfluentialPeptide Interference with APP and Tau Association: Relevance to Alzheimer’s Disease Amelioration
Maron, R., Armony, G., Tsoory, M., Wilchek, M., Frenkel, D., & Arnon, R. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21093270 · Cited by 13
“The Y-maze test [47] consists of two trials, first “training” and second “retention”, separated by an inter-trial interval (ITI).”
MethodPotential learning and memory disruptors and enhancers in a simple, 1-day operant task in mice
Sanku, R. K. K., John, J., Salkovitz, M., Ilies, M. A., & Walker, E. A. (2018) · Behavioural Pharmacology · doi:10.1097/fbp.0000000000000400 · Cited by 12
Piscitelli, F., Coccurello, R., Totaro, A., Leuti, A., Giacovazzo, G., Verde, R., Rossi, E., Vulpiani, M. P., Ferri, N., Stuffler, R. G., et al. (2019) · European Journal of Lipid Science and Technology · doi:10.1002/ejlt.201900015 · Cited by 12
Acharya, N. K., Grossman, H. C., Clifford, P. M., Levin, E. C., Light, K., Choi, H.-N., Swanson, R. L., Kosciuk, M. C., Venkataraman, V., Libon, D. J., et al. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-231028 · Cited by 13
“These five tasks were chosen based on their suggested sensitivity to AD-related pathologies and/or their conceptual relevance to cognitive impairments associated with AD [78, 79].”
BackgroundMethodJoseph, D. J., Liu, C., Peng, J., Liang, G., & Wei, H. (2019) · PLoS ONE · doi:10.1371/journal.pone.0223509 · Cited by 11
Stimmell, A. C., Xu, Z., Moseley, S. C., Cushing, S. D., Fernández, D. M. V., Dang, J. V., Santos-Molina, L. F., Anzalone, R. A., Garcia-Barbon, C. L., Rodriguez, S., et al. (2021) · Frontiers in Aging · doi:10.3389/fragi.2021.655015 · Cited by 11
“A large body of work, including our own, has found that rodents that recapitulate neurodegenerative features of AD have similar spatial navigation impairments (e.g., Cacucci et al., 2008; Attar et al., 2013; Liu et al., 2013; Marlatt et al., 2013; Webster et al., 2014; Zhao et al., 2014; Stimmell et al., 2019; Cushing…”
BackgroundIachini, T., Ruotolo, F., Iavarone, A., Mazzi, M. C., & Ruggiero, G. (2021) · Brain Sciences · doi:10.3390/brainsci11111536 · Cited by 12
Organotypic Cultures as a Model to Study Adult Neurogenesis in CNS Disorders
Cavaliere, F., Benito‐Muñoz, M., & Matute, C. (2016) · Stem Cells International · doi:10.1155/2016/3540568 · Cited by 13
“AD ismimicked by different animalmodels from invertebrate [37] to rodents [38].”
Zhang, S., & Sehgal, A. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-812536-6.00011-0 · Cited by 12
Hascup, K. N., Britz, J., Findley, C. A., Tischkau, S. A., & Hascup, E. R. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-181231 · Cited by 13
“To test the procognitive effects of mGluR2/3 activation, LY379268 intervention began prior to the onset of cognitive deficits that have been reported as early as 6–8 months [63, 64] and continue throughout the lifespan of AβPP/PS1 mice [28].”
Eom, T.-M., Kwon, H. H., Shin, N., Kim, D. W., Fang, Z., Seol, I.-C., Kim, Y.-S., Kim, H.-G., & Yoo, H.-R. (2020) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2020.113102 · Cited by 12
Increased Insoluble Amyloid-β Induces Negligible Cognitive Deficits in Old AppNL/NL Knock-In Mice
Salas, I. H., Callaerts-Vegh, Z., D’Hooge, R., Saido, T. C., Dotti, C. G., & De Strooper, B. (2018) · Journal of Alzheimer's Disease · doi:10.3233/jad-180410 · Cited by 12
“Previous models for AD displayed an increased locomotor activity [15].”
BackgroundZhang, T., Musheshe, N., van der Veen, C. H. T. J., Kessels, H. W. H. G., Dolga, A. M., Deyn, P. P. D., Eisel, U. L. M., & Schmidt, M. (2023) · Biomedicines · doi:10.3390/biomedicines11082096 · Cited by 11
“In order to investigate how Aβ contributes to AD pathology, several AD transgenic models, such as APP/PS1 and J20, were developed overexpressing Aβ precursor protein (APP) and displaying early memory deficits [7].”
BackgroundCholinergic cognitive enhancer effect of Salvia triloba L. essential oil inhalation in rats
ERTOSUN, G. B., Ergen, M., Bardakçı, H., Barak, T. H., & Süyen, G. G. (2023) · Marmara medical journal · doi:10.5472/marumj.1368345 · Cited by 11
Development of a 3D tracking system for multiple marmosets under free-moving conditions
Yurimoto, T., Kumita, W., Sato, K., Kikuchi, R., Oka, G., Shibuki, Y., Hashimoto, R., Kamioka, M., Hayasegawa, Y., Yamazaki, E., et al. (2024) · Communications Biology · doi:10.1038/s42003-024-05864-9 · Cited by 10
Callaerts‐Vegh, Z., Ahmed, T., Vermaercke, B., Marynen, P., Balschun, D., Froyen, G., & D’Hooge, R. (2015) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2015.00179 · Cited by 11
“We observed no influence of Nxf7 deficiency on single-trial passive avoidance learning, a test that relies on simple contextual association (Bartus et al., 1980; Gower and Lamberty, 1993; Webster et al., 2014).”
BackgroundFatima, F., Rizvi, D. A., Abidi, A., Ahmad, A., Shukla, P., Qadeer, F., & Srivastava, K. (2017) · International Journal of Basic & Clinical Pharmacology · doi:10.18203/2319-2003.ijbcp20172747 · Cited by 11
“As soon as the rat climbed the pole, both the buzzer and foot-shock were switched off.(18,19) Escape latency in seconds was recorded as end point measure.”
BackgroundObject Novelty Recognition Memory
Ennaceur, A. (2018) · Handbook of behavioral neuroscience · doi:10.1016/b978-0-12-812012-5.00001-x · Cited by 11
Maglione, A., do Nascimento, B. P. P., Ribeiro, M. O., de Souza, T. J. L., da Silva, R. E. C., Sato, M. A., Penatti, C. A. A., Britto, L. R., de Souza, J. S., Maciel, R. M. B., et al. (2022) · Metabolic Brain Disease · doi:10.1007/s11011-022-01055-9 · Cited by 11
“A previous study showed that at six months-old, these animals already developed associative learning and spatial working memory deficits, as well as an impairment in contextual fear conditioning (Webster et al., 2014).”
BackgroundLiang, C., Nguyen, G. A. H., Danh, T. B., Sandhu, A. K., Melkonyan, L. L., Syed, A. U., & Mukherjee, J. (2023) · Synapse · doi:10.1002/syn.22265 · Cited by 11
“Transgenic mice models allow the study of specific pathology such as Aβ plaques in AD (Webster et al., 2014).”
BackgroundMhillaj, E., Cuomo, V., & Mancuso, C. (2017) · Behavioural Pharmacology · doi:10.1097/fbp.0000000000000296 · Cited by 11
“whereas an impairment in working memory occurred very late and became consistent by 15 months of age (Webster et al., 2014).”
BackgroundThe single-use rhinolaryngoscope: an evaluation and cost comparison
Mistry, R., Russell, R. V., Walker, N., & Ofo, E. (2020) · The Journal of Laryngology & Otology · doi:10.1017/s0022215120001656 · Cited by 11
Systems genetics identifies modifiers of Alzheimer’s disease risk and resiliencePreprint
Neuner, S. M., Hohman, T. J., Richholt, R., Bennett, D. A., Schneider, J. A., Jager, P. L. D., Huentelman, M. J., O’Connell, K. M. S., & Kaczorowski, C. C. (2017) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/225714 · Cited by 11
“As deficits in working memory performance in AD mouse models most closely parallels the earliest AD-related cognitive deficits detected in humans during the late preclinical phase of the disease (Webster et al., 2014), these gene candidates represent new targets to delay the onset of disease.”
BackgroundO’Leary, T. P., & Brown, R. E. (2024) · Behavioural Brain Research · doi:10.1016/j.bbr.2024.114970 · Cited by 11
“Despite the number of age-related impairments in “ non-cognitive ” sensory, motor and neuropsychiatric symptoms reported in AD patients, assessment of behavior in AD mouse models has traditionally focused on impairments in cognitive function (i.e., learning and memory ability) [4, 5,23,61,73,113].”
Microglial Responses to Alzheimer's Disease Pathology: Insights From “Omics” Studies
Reid, A. N., Jayadev, S., & Prater, K. E. (2025) · Glia · doi:10.1002/glia.24666 · Cited by 10
“…1997], APP V717I [London; Goate et al. 1991]) and two in PSEN1 (PSEN1 M146L and L286V) are combined to generate a model that develops amyloid plaques as early as 10 weeks of age and present with significant cognitive deficits as early as 3 months of age (Oakley et al. 2006; Webster et al. 2014).”
Lead Optimization of a Butyrylcholinesterase Inhibitor for the Treatment of Alzheimer’s Disease
Košak, U., Benedik, N. S., Knez, D., Žakelj, S., Trontelj, J., Pišlar, A., Horvat, S., Bolje, A., Žnidaršič, N., Grgurevič, N., et al. (2025) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.5c00577 · Cited by 12
Scaffold-Assisted Ectopic Transplantation of Internal Organs and Patient-Derived Tumors
Carpenter, R., Oh, H. J., Ham, I., Kim, D., Hur, H., & Lee, J. (2019) · ACS Biomaterials Science & Engineering · doi:10.1021/acsbiomaterials.9b00978 · Cited by 11
Cognitive improvement via cortical cannabinoid receptors and choline‐containing lipids
Moreno‐Rodríguez, M., Martínez‐Gardeazabal, J., de Tena, I. B., Llorente‐Ovejero, A., Lombardero, L., Román, E. G. D. S., Giménez‐Llort, L., Manuel, I., & Rodríguez‐Puertas, R. (2024) · British Journal of Pharmacology · doi:10.1111/bph.17381 · Cited by 9
“Although cognitive functions are already affected at this stage due to the onset of AD pathology in the 3xTg-AD mice (Belfiore et al., 2019; Muntsant et al., 2023), it appears that the cognitive deficits as measured by BM, are manifested later in disease progression (Webster et al., 2014).”
A call for new approaches to Alzheimer's disease research
Coleman, P. D., & Mastroeni, D. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.04.027 · Cited by 10
“, plaques and tangles) features of human AD (Webster et al., 2014).”
BackgroundLi, N., Hu, P., Xu, T., Chen, H., Chen, X., Hu, J., Yang, X., Shi, L., Luo, J., & Xu, J. (2017) · Current Alzheimer Research · doi:10.2174/1567205014666170719165745 · Cited by 11
Oroszi, T., Geerts, E., Rajadhyaksha, R., Nyakas, C. J., van Heuvelen, M. J. G., & van der Zee, E. A. (2023) · Behavioral and Brain Functions · doi:10.1186/s12993-023-00208-9 · Cited by 9
Montgomery, K. S., Edwards, G. A., Levites, Y., Kumar, A., Myers, C. E., Gluck, M. A., Setlow, B., & Bizon, J. L. (2015) · Hippocampus · doi:10.1002/hipo.22535 · Cited by 10
“…water maze, and Barnes maze) are typically not evident until well after 6 months of age (Lalonde et al., 2004; Reiserer et al., 2007; Volianskis et al., 2010; Cramer et al., 2012), with deficits across tasks becoming more reliable at quite advanced ages (i.e., >15 months, (Webster et al., 2014)).”
BackgroundFongsaran, C., Jirakanwisal, K., Peng, B.-H., Fracassi, A., Taglialatela, G., Dineley, K. T., Paessler, S., & Cisneros, I. E. (2024) · Brain, Behavior, & Immunity - Health · doi:10.1016/j.bbih.2024.100780 · Cited by 9
“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).”
BackgroundMethodDevelopment of an anti-tauopathy mucosal vaccine specifically targeting pathologic conformers
Tan, W., Thiruppathi, J., Hong, S. H., Puth, S., Pheng, S., Mun, B.-R., Choi, W., Lee, K., Park, H., Nguyen, D. T., et al. (2024) · npj Vaccines · doi:10.1038/s41541-024-00904-1 · Cited by 10
“The NORT evaluates recognition memory, and the Y-maze tests assess reference memory and working memory 69 .”
MethodO’Hare, N. R., Millican, K., & Ebong, E. E. (2024) · Frontiers in Physiology · doi:10.3389/fphys.2024.1394725 · Cited by 10
Guan, R., Xue, Z., Huang, K., Zhao, Y., He, G., Dai, Y., Liang, M., Wen, Y., Ye, X., Liu, P., et al. (2025) · Pharmaceuticals · doi:10.3390/ph18081080 · Cited by 10
“The passive avoidance task was used to evaluate associative learning and memory based on aversive stimuli [42].”
Gharedaghi, M. H., Rahimian, R., Dehpour, A. R., Yousefzadeh-fard, Y., & Mohammadi-Farani, A. (2015) · Psychopharmacology · doi:10.1007/s00213-015-3950-x · Cited by 8
Tsuda, L., Omata, Y., Yamasaki, Y., Minami, R., & Lim, Y. (2017) · Human Molecular Genetics · doi:10.1093/hmg/ddx346 · Cited by 9
Park, S., & Han, K. S. (2022) · Current Alzheimer Research · doi:10.2174/1567205019666220404104854 · Cited by 9
Tortuyaux, R., Avila‐Gutierrez, K., Oudart, M., Mazaré, N., Mailly, P., Deschemin, J., Vaulont, S., Escartin, C., & Cohen‐Salmon, M. (2022) · Journal of Neurochemistry · doi:10.1111/jnc.15747 · Cited by 10
Choi, M., Jang, H.-S., Son, T., Kim, D., Youn, Y.-J., Hwang, G.-B., Choi, Y. P., & Jeong, Y. H. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242015064 · Cited by 9
“In addition to the Y-maze, NOR test, and LAB-ORAS test, other tests such as the T-maze, Morris water maze (MWM), contextual fear conditioning test, rotarod, elevated plus maze, eight-arm radial maze, and Barnes maze are also commonly used in AD research [11–14].”
MethodEslamizade, M. J., Madjd, Z., Rasoolijazi, H., Saffarzadeh, F., Pirhajati, Aligholi, H., Janahmadi, M., & Mehdizadeh, M. (2016) · Europe PMC (PubMed Central) · Cited by 9
Yao, Y., Huang, J., Chen, L., Chen, Y., & Li, X. (2017) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2017.5182 · Cited by 9
Oberman, K., Gouweleeuw, L., Hoogerhout, P., Eisel, U. L. M., van Riet, E., & Schoemaker, R. G. (2020) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-200213 · Cited by 9
Experimental Approach to Alzheimer’s Disease with Emphasis on Insulin Resistance in the Brain
Šalković‐Petrišić, M., Perhoč, A. B., Homolak, J., Knezović, A., Barilar, J. O., & Riederer, P. F. (2021) · Springer eBooks · doi:10.1007/978-3-030-71519-9_98-1 · Cited by 9
Savonenko, A. V., Wong, P. C., & Li, T. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-85654-6.00022-8 · Cited by 8
Motor Cortex Theta and Gamma Architecture in Young Adult APPswePS1dE9 Alzheimer Mice
Papazoglou, A., Soós, J., Lundt, A., Wormuth, C., Ginde, V. R., Müller, R., Henseler, C., Broich, K., Xie, K., Haenisch, B., et al. (2017) · PLoS ONE · doi:10.1371/journal.pone.0169654 · Cited by 10
“Numerous transgenic mouse models of AD supposed to fulfill the criteria of homology, isomorphism and predictability have been generated in the past [11, 12].”
BackgroundResearch on Alzheimer's Disease (AD) Involving the Use of In vivo and In vitro Models and Mechanisms
Sinha, S., Wal, P., Prakash Goudanavar, S. O. P., Divya, S., Kimothi, V., Jyothi, D., Sharma, M. C., & Wal, A. (2024) · Central Nervous System Agents in Medicinal Chemistry · doi:10.2174/0118715249293642240522054929 · Cited by 9
Raduan, S. Z., Ahmed, Q. U., Rusmili, M. R. A., Sabere, A. S. M., Haris, M. S., Shaikh, M. F., Sulaiman, W. A. W., & Mahmood, M. H. (2024) · Neurology Perspectives · doi:10.1016/j.neurop.2024.100180 · Cited by 8
Turton, S. M., Padgett, S., Jessup, M. T., Johnson, C. E., Buzinova, V. A., Barth, S. E., Köhler, K., Spearman, H. M., Macheda, T., Manauis, E. C., et al. (2025) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2025.167840 · Cited by 7
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“Middle-aged APP/PS1 mice display deficits in learning and memory function (Webster et al. 2014).”
Cognitive Phenotypes for Biomarker Identification in Mental Illness: Forward and Reverse Translation
MacQueen, D. A., Young, J. W., & Cope, Z. A. (2018) · Current topics in behavioral neurosciences · doi:10.1007/7854_2018_50 · Cited by 8
Liu, J., Zhang, C., Wang, J., Huang, Y., Shen, D., Hu, Y., Chu, H., Yu, X., Zhang, L., & Ma, H. (2022) · Pharmaceuticals · doi:10.3390/ph15121481 · Cited by 8
“Studies have shown that cognitive deficits are observed in APPswe/PS1dE9 (APP/PS1) transgenic mice at the age of three months in the radial arm water maze (RAWM) spatial working memory task, and are also seen at six months of age in the Morris water maze (MWM) [9].”
BackgroundLiu, L.-Z., Fan, S., Gao, J., Li, W., & Xian, X. (2023) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2023.110683 · Cited by 9
“The model starts producing amyloid plaques from five months old, with peak production occurring at 12 months old, and exhibits pathological manifestations consistent with AD (Webster et al. 2014).”
BackgroundMoradi, F., van den Berg, M., Mirjebreili, S. M., Kosten, L., Verhoye, M., Amiri, M., & Keliris, G. A. (2023) · iScience · doi:10.1016/j.isci.2023.107454 · Cited by 9
“Previous studies that characterized in detail the pathophysiology of this animal model, have indicated its great potential over other murinemodels.(54,55) Very importantly, the relatively slow disease progression dynamics in this model that simulate different stages of AD in humans, offer remarkable opportunities for…”
ResultCognitive trajectories in longitudinally trained 3xTg-AD mice
Duggan, M. R., Steinberg, Z. R., Peterson, T., Francois, T.-J., & Parikh, V. (2023) · Physiology & Behavior · doi:10.1016/j.physbeh.2023.114435 · Cited by 8
Zheng, M., Zhang, B., Yau, S. S. Y., So, K., Zhang, L., & Ou, H. (2024) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-23-01101 · Cited by 8
Endres, K., Reinhardt, S., Geladaris, A., Knies, J., Grimm, M. O. W., Hartmann, T., & Schmitt, U. (2016) · BMC Neuroscience · doi:10.1186/s12868-016-0280-9 · Cited by 9
“Double, triple or even quintuple transgenic mice have been established with combination of each gene to overcome low intensity and long time frame of progression of pathological hallmarks (for a characterization of 10 such models see: [2]).”
InfluentialBretin, S., Krazem, A., Henkous, N., Froger-Colléaux, C., Mocaër, E., Louis, C., Perdaems, N., Marighetto, A., & Béracochéa, D. (2017) · Psychopharmacology · doi:10.1007/s00213-017-4792-5 · Cited by 8
“The most widely used paradigms for working memory are maze type tasks (Webster et al. 2014).”
MethodDose-dependent neuroprotective effect of the JNK inhibitor Brimapitide in 5xFAD transgenic mice
Porte, B., Marguerit, G., Thomasseau, S., Paquet, C., & Hugon, J. (2019) · Brain Research · doi:10.1016/j.brainres.2019.146587 · Cited by 8
Timing impairments in early Alzheimer’s disease: Evidence from a mouse model.
Armstrong, P., Pardon, M., & Bonardi, C. (2020) · Behavioral Neuroscience · doi:10.1037/bne0000359 · Cited by 7
“For example, spatial learning is impaired in both AD and MCI (Allison et al., 2016, Verghese et al., 2017, Laczo et al., 2009, Vlcek and Laczo, 2014), an effect mirrored in virtually all transgenic mouse models of AD (Stewart et al., 2011, Webster et al., 2014).”
BackgroundAlterations of fatty acid composition and metabolism in APP/PS1 transgenic mice
Bai, Y.-R., Wang, Y., Meng, D., Shi, Z.-L., Song, X., Yang, Z., Zhang, W., Yang, L., & Shi, R. (2020) · Neuroscience Letters · doi:10.1016/j.neulet.2020.135401 · Cited by 8
Maigler, K. C., Buhr, T. J., Park, C. S., Miller, S. A., Kozlowski, D. A., & Marr, R. A. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2020.6989 · Cited by 8
“and memory, which is a hippocampal-dependent task that is affected in both TBI and AD models.(54,60) Mice were trained to”
Svensson, M., Olsson, G., Yang, Y., Bachiller, S., Ekemohn, M., Ekstrand, J., & Deierborg, T. (2021) · Scientific Reports · doi:10.1038/s41598-021-83998-0 · Cited by 8
Impairment of visual cortical plasticity by amyloid-beta species
William, C. M., Stern, M., Pei, X., Saqran, L., Ramani, M. D., Frosch, M. P., & Hyman, B. T. (2021) · Neurobiology of Disease · doi:10.1016/j.nbd.2021.105344 · Cited by 9
Luo, Y., Sun, Y., Wen, H., Wang, X., Zheng, X., Ge, H., Yi, Y., Wu, X., Li, W., & Hou, W. (2023) · Journal of Applied Biomedicine · doi:10.1016/j.bbe.2022.12.010 · Cited by 8
Zhou, X. J., Huang, J., Pan, S., Xu, M., He, R., Ji, Z., & Hu, Y. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160191 · Cited by 8
Precise relative-quantity judgement in the striped field mouse Apodemus agrarius Pallas
Reznikova, Z. I., Panteleeva, S. N., & Vorobyeva, N. S. (2019) · Animal Cognition · doi:10.1007/s10071-019-01244-7 · Cited by 8
Schlunk, F., Fischer, P., Princen, H. M. G., Rex, A., Prinz, V., Foddis, M., Lütjohann, D., Laufs, U., & Endres, M. (2021) · Behavioural Brain Research · doi:10.1016/j.bbr.2020.112875 · Cited by 10
Flores-Cuadra, J. A., Madrid, A., Fernández, P. L., Perez-Lao, A. R., Oviedo, D. C., Britton, G. B., & Carreira, M. B. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200870 · Cited by 9
“Most studies do not analyze behavioral psychological symptoms of dementia, such as depression, anxiety and sleep disturbances, important components of clinical symptoms [8, 9].”
InfluentialGnanaprakash, M., Staniszewski, A., Zhang, H., Pitstick, R., Kavanaugh, M. P., Arancio, O., & Nicholls, R. E. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-200462 · Cited by 9
“The Tg2576 transgene encodes a 695 amino acid form of human APP carrying the Swedish (K670N, M671L) mutation under the control of the hamster prion protein promoter, and animals that carry this transgene exhibit well-characterized behavioral and electrophysiological impairments [34, 35].”
BackgroundSpicer, M. M., Yang, J., Fu, D., DeVore, A. N., Lauffer, M., Sayar, N., Atasoy, D., & Fisher, R. A. (2024) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-23-01993 · Cited by 9
“Working memory is one of the most well-modeled memory deficits in AD, and the most widely used paradigms in mice are maze-tasks which require spatial working memory to solve (Webster et al., 2014).”
Möller, J. E. L., Schmitt, F. W., Günther, D., Stöver, A., & Bouter, Y. (2024) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2024.173944 · Cited by 9
“Memory impairments are a characteristic symptom of AD, and like-wise, age-dependent deficits in memory and learning are observed in 5XFAD mice (Oblak et al., 2021; Sanchez et al., 2023; Webster et al., 2014).”
Self-citationZarneshan, S. N., Fakhri, S., Kiani, A., Abbaszadeh, F., Hosseini, S. Z., Noori, E. M., & Echeverría, J. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1574323 · Cited by 7
Wang, X., Wang, Y., Zhang, J., Li, Q., Yu, T., & Yang, Y. (2025) · Phytomedicine · doi:10.1016/j.phymed.2025.157161 · Cited by 7
Zurlinden, T. J., & Reisfeld, B. (2018) · Environmental Health Perspectives · doi:10.1289/ehp1743 · Cited by 7
Adropin transgenesis improves recognition memory in diet-induced obese LDLR-deficient C57BL/6J mice
Ghoshal, S., Banerjee, S., Zhang, J., Niehoff, M. L., Farr, S. A., & Butler, A. A. (2021) · Peptides · doi:10.1016/j.peptides.2021.170678 · Cited by 7
Zhao, Y., Bao, J., Liu, W., Gong, X., Liang, Z., Li, W., Wu, M., Xiao, Y., Sun, B., Wang, X., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-215016 · Cited by 6
“In APP/PS1 mice, long-term memory is impaired at 6-to 8-month-old as the amyloid burden increases and deteriorates synaptic plasticity [52, 53].”
Phytochemical based Modulation of Endoplasmic Reticulum Stress in Alzheimer's Disease
Dsouza, V. L., Shivakumar, A. B., Kulal, N., Gangadharan, G., Kumar, D., & Kabekkodu, S. P. (2022) · Current Topics in Medicinal Chemistry · doi:10.2174/1568026622666220624155357 · Cited by 8
McFadden, S., Sime, L. N., Cox, M. F., Findley, C. A., Peck, M. R., Quinn, K., Fang, Y., Bartke, A., Hascup, E. R., & Hascup, K. N. (2022) · The Journals of Gerontology Series A · doi:10.1093/gerona/glac223 · Cited by 7
“Learning and memory recall deficits in APP/PS1 mice are routinely observed by 12 months of age (24,25).”
BackgroundBehavioral and transcriptomic effects of the cancer treatment tamoxifen in mice
Galvano, E., Pandit, H., Sepulveda, J., Ng, C. A. S., Becher, M. K., Mandelblatt, J. S., Dyk, K. V., & Rebeck, G. W. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1068334 · Cited by 7
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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