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Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models
Open accessAbstract
The goal of this review is to discuss how behavioral tests in mice relate to the pathological and neuropsychological features seen in human Alzheimer's disease (AD), and present a comprehensive analysis of the temporal progression of behavioral impairments in commonly used AD mouse models that contain mutations in amyloid precursor protein (APP). We begin with a brief overview of the neuropathological changes seen in the AD brain and an outline of some of the clinical neuropsychological assessments used to measure cognitive deficits associated with the disease. This is followed by a critical assessment of behavioral tasks that are used in AD mice to model the cognitive changes seen in the human disease. Behavioral tests discussed include spatial memory tests [Morris water maze (MWM), radial arm water maze (RAWM), Barnes maze], associative learning tasks (passive avoidance, fear conditioning), alternation tasks (Y-Maze/T-Maze), recognition memory tasks (Novel Object Recognition), attentional tasks (3 and 5 choice serial reaction time), set-shifting tasks, and reversal learning tasks. We discuss the strengths and weaknesses of each of these behavioral tasks, and how they may correlate with clinical assessments in humans. Finally, the temporal progression of both cognitive and non-cognitive deficits in 10 AD mouse models (PDAPP, TG2576, APP23, TgCRND8, J20, APP/PS1, TG2576 + PS1 (M146L), APP/PS1 KI, 5×FAD, and 3×Tg-AD) are discussed in detail. Mouse models of AD and the behavioral tasks used in conjunction with those models are immensely important in contributing to our knowledge of disease progression and are a useful tool to study AD pathophysiology and the resulting cognitive deficits. However, investigators need to be aware of the potential weaknesses of the available preclinical models in terms of their ability to model cognitive changes observed in human AD. It is our hope that this review will assist investigators in selecting an appropriate mouse model, and accompanying behavioral paradigms to investigate different aspects of AD pathology and disease progression.
Overview
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Written from the paper’s full text.
TL;DR
This review maps how behavioral tasks used in amyloid precursor protein (APP) mutant mice correspond to the neuropsychological assessments used clinically in Alzheimer's disease (AD), and tabulates the temporal onset of cognitive and non-cognitive deficits across 10 commonly used AD mouse models. It concludes that no single model recapitulates human AD, but that most models show spatial working memory deficits earlier than deficits in other cognitive domains.
Key findings
- Across the reviewed models, the earliest observable cognitive impairment is consistently in spatial working memory (assessed by water maze tasks), generally followed by associative learning/reference memory deficits, with recognition memory deficits appearing later (e.g., PDAPP: working memory at 4 months, NOR at 6 months; Tg2576: spatial working memory at 5 months, NOR at 12 months; APP/PS1 KI: RAWM at 9 months, recognition memory at 15 months).
- Onset varies substantially by model: J20 shows recognition memory deficits earliest (1–2 months), while APP/PS1 KI shows the latest onset (7–9 months for earliest deficits).
- Non-cognitive abnormalities are also present in most models, including increased locomotor activity (J20 and TgCRND8 earliest at ~1 month; PDAPP and Tg2576 at ~3 months; PS1, 3×Tg-AD, and APP23 at ~6–9 months), anxiety, circadian/sleep disruption, and aggression (e.g., APP23 aggression by 6 months).
- The review notes that increased aggression presents in as much as 65% of AD patients, and that depressive symptom prevalence in AD is reported to range from 2% to 85%, though little work has examined depressive-like behavior in AD mouse models.
Methods
- Narrative review, not primary experimental work: it summarizes human AD neuropathology (ABC scoring of Amyloid, Braak, CERAD), clinical neuropsychological instruments (MMSE, MoCA, SBT, ADAS-cog, Logical Memory I/II, BVRT), and mouse behavioral tasks (MWM, RAWM, Barnes maze, Y-/T-maze, NOR, fear conditioning, passive/active avoidance, DMTP/DMTS, 3- and 5-CSRTT, set-shifting, reversal learning, WWWhich).
- The core synthesis is two tables (Table 3 for five APP models: PDAPP, TG2576, APP23, TgCRND8, J20; Table 4 for five APP+PS1/Tau models: APP/PS1, TG2576+PS1(M146L), APP/PS1 KI, 5×FAD, 3×Tg-AD) coding impairment, no impairment, or no data by age, with an asterisk marking first appearance of diffuse amyloid plaques.
- No new data, sample sizes, or statistical analyses are reported; findings are drawn from cited primary studies.
Limitations
- Stated by the paper: no animal model recapitulates the entirety of AD; most models represent familial AD (FAD), which accounts for only a small percentage of total AD cases; background strain and likely overexpression of mutant human APP genes on brain development and function must always be considered; language-dependent domains (verbal acuity, verbal recall) cannot be modeled in rodents; the WWWhich episodic-like memory task is not comparable to human episodic memory tests because those rely on language; homology between rodent and human 5-CSRTT is "far from perfect."
- Stated by the paper: the tables are not an all-encompassing list of mouse models, only examples of commonly used APP-mutation models.
- Evident from the text: the tables contain many cells with no available data, and the review documents inconsistent reports across studies for several models (e.g., Tg2576 spatial memory deficits not replicated in some reports; PDAPP recognition memory findings inconsistent), indicating that model-by-model progression claims rest on heterogeneous and sometimes conflicting literature.
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In the paper
“Similar to the reported activity disturbances, circadian rhythm disruptions are also observed in many of the AD mouse models”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Circadian rhythm and sleep disruptions
What the sources say
- Not checked yetcites Huitron-Resendiz et al., 2002
- Not checked yetcites Vloeberghs et al., 2004
- Not checked yetcites Wisor et al., 2005
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Other models such as the TG2576 develop the anxiety-like disturbances later at the age of 9–11 months of age”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
What the sources say
- Not checked yetcites Gil-Bea et al., 2007
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“not all murine AD models exhibit anxiety disturbances”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
What the sources say
- Not checked yetcites Arendash et al., 2001b
- Not checked yetcites Lalonde et al., 2002
- Not checked yetcites Webster et al., 2013
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Many AD mouse models also display increased aggressive behavior”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Moechars et al., 1996
- Not checked yetcites Van Dorpe et al., 2000
- Not checked yetcites Ambree et al., 2006 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Several mouse models of AD also display sleep disruption.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Circadian rhythm and sleep disruptions
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“These aggressive disruptions appear to develop later than the onset of cognitive deficits in this model”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Kelly et al., 2003
- Not checked yetcites Van Dam et al., 2003
- Not checked yetcites Vloeberghs et al., 2006
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Anxiety disturbances have been reported in many of the AD mouse models”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
What the sources say
- Not checked yetcites Moechars et al., 1996
- Not checked yetcites Lalonde et al., 2003
- Not checked yetcites Gil-Bea et al., 2007
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Still, the majority of models do display these disturbances”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“The APP23 mouse model of AD also shows increased aggressive behaviors”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Vloeberghs et al., 2006
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The temporal time course of these anxiety-like disturbances can vary depending on the mouse model.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- It may state two separate claims as one. 41
- The quote only partly states this claim. 1
- Probably not a substantial claim. 24
None of the sources cited for this claim have been checked yet.
In the paper
“The onset of the disturbances is different for each model, with the J20 and the TgCRND8 mice developing disruptions earliest (approximately 1 month of age), followed by PDAPP and TG2576 (approximately 3 months of age), and the PS1 [Tg2576 + PS1 (M146L)], 3×TgAD, and APP23 mice developing last (approximately 6–9 months of age)”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Locomotor activity
What the sources say
- Not checked yetcites Dodart et al., 1999
- Not checked yetcites King et al., 1999
- Not checked yetcites Arendash et al., 2001b
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Other AD mouse models that show activity disturbances are the PDAPP, TG2576, J20, APP + PS1 [Tg2576 + PS1 (M146L)], and 3×Tg-AD mouse models of AD.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Locomotor activity
What the sources say
- Not checked yetcites Dodart et al., 1999
- Not checked yetcites King et al., 1999
- Not checked yetcites Arendash et al., 2001b
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“the greater the sleep disruptions are, the more severe the cognitive decline seems to be”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Circadian rhythm and sleep disruptions
What the sources say
- Not checked yetcites Huitron-Resendiz et al., 2002
- Not checked yetcites Huitron-Resendiz et al., 2005
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
In the paper
“in the TG2576 mouse increased aggressive behaviors display themselves in both the frequency of attacks on other home cage mice as well as on the latency to first attack when interacting with a novel mouse”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Alexander et al., 2011 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“in some models the behavioral disturbances start early at 1–2 months of age or 3–6 months of age for the J20 and the APP/PS1 models, respectively”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Anxiety disturbances
What the sources say
- Not checked yetcites Lalonde et al., 2004
- Not checked yetcites Reiserer et al., 2007
- Not checked yetcites Harris et al., 2010
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“most of the studies using mouse models of AD have focused on understanding/correcting the cognitive deficits associated with the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Conclusions
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“NFTs spread to the limbic and medial temporal lobe (Braak stage III-IV), and this stage correlates with early AD symptoms related to memory (Schmitt et al., 2000; Riley et al., 2011).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Overview of neuropathological changes in AD
What the sources say
- Not checked yetcites Schmitt et al., 2000
- Not checked yetcites Riley et al., 2011
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Because the ADAS-cog has an excellent test-retest reliability and is considered to be one of the most sensitive scales for assessing cognitive changes related to AD (Emilien et al., 2004), this test is extensively used in AD clinical trials as an outcome measure of cognitive change (Schmitt and Wichems, 2006; Connor and Sabbagh, 2008).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Emilien et al., 2004
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Because the ADAS-cog has an excellent test-retest reliability and is considered to be one of the most sensitive scales for assessing cognitive changes related to AD (Emilien et al., 2004), this test is extensively used in AD clinical trials as an outcome measure of cognitive change (Schmitt and Wichems, 2006; Connor and Sabbagh, 2008).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Schmitt and Wichems, 2006
- Not checked yetcites Connor and Sabbagh, 2008
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The MMSE has excellent reproducibility that lends itself well to longitudinal use in tracking the progression of the cognitive impairments associated with AD (Jacqmin-Gadda et al., 1997; Aevarsson and Skoog, 2000; Chatfield et al., 2007).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Jacqmin-Gadda et al., 1997
- Not checked yetcites Aevarsson and Skoog, 2000 source
- Not checked yetcites Chatfield et al., 2007
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Another commonly used test battery is that of the Short Blessed Test (SBT) which consists of a six-item test designed to identify the cognitive dysfunction seen in AD (Katzman et al., 1983).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Katzman et al., 1983
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Despite the simplicity and brevity of the SBT, the results that it produces have demonstrated excellent reliability (Fuld, 1978).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Fuld, 1978
Strength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Similarly, the SBT was the first mental status examination to be correlated with amyloid plaque burden at autopsy (Carpenter et al., 2011).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Carpenter et al., 2011
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The Mini-Mental Status Examination (MMSE) is one of the most commonly used neuropsychological screening tools for cognitive impairments seen in AD (Simard and Van Reekum, 1999; Snyderman and Rovner, 2009).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Simard and Van Reekum, 1999
- Not checked yetcites Snyderman and Rovner, 2009
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The data also support the “Amyloid Cascade Hypothesis”(Karran et al., 2011), a deceptively complex hypothesis which posits that beta-amyloid/plaque pathology kindles widespread tau/NFT pathology, with the tau/NFT pathology constituting the more direct cause of the cell loss and synapse elimination underlying clinical disease (Nelson et al., 2009b, 2012).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Overview of neuropathological changes in AD
What the sources say
- Not checked yetcites Karran et al., 2011
- Not checked yetcites Nelson et al., 2009b
- Not checked yetcites Nelson et al., 2012
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Outside of frontotemporal lobar degeneration (FTLD), one does not see widespread cortical NFTs without abundant plaque pathology.
In the paper
“The Alzheimer's Disease Assessment Scale (ADAS) was specifically developed to measure the severity of symptoms commonly seen in AD (Rosen et al., 1984).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Mental status exams
What the sources say
- Not checked yetcites Rosen et al., 1984
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“These tasks rely on the natural exploratory behavior (tendency to choose an alternative arm over an arm which has been previously explored) of rodents and are considered the most rudimentary tasks to assess spatial working memory (Dudchenko, 2004).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Dudchenko, 2004
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Once the AD patient progresses past MCI and into dementia, general cognition continues to decline with deficits appearing in all respective cognitive domains (Huff et al., 1987; Locascio et al., 1995; Lambon Ralph et al., 2003; Mckhann et al., 2011).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Cognitive neuropsychological assessment summary
What the sources say
- Not checked yetcites Huff et al., 1987
- Not checked yetcites Locascio et al., 1995
- Not checked yetcites Lambon Ralph et al., 2003
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Large numbers of AD mouse models have been tested in the MWM and most show AD related cognitive deficits (Webster et al., 2013).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Webster et al., 2013
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Instead, spatial based working memory tasks are heavily employed in murine working memory testing and likely are more depictive of the visuospatial working memory tasks used clinically (Benton, 1992; Benedict and Groninger, 1994).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Benton, 1992
- Not checked yetcites Benedict and Groninger, 1994
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Working memory is perhaps one of the most well modeled aspects of the memory deficits in AD.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Some cognitive domains disrupted in AD have been extensively modeled (reference memory, working memory and executive function), some less so (attention), and some nearly not at all (episodic memory).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD?
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Other cognitive domains impaired in human AD such as those involving language (i.e., verbal acuity tasks and verbal recall tasks) simply cannot be modeled in rodent models.
None of the sources cited for this claim have been checked yet.
In the paper
“Clinically, many of the neuropsychological tests that assess working memory rely heavily on the use of verbal tasks (Kaplan et al., 1978; Benedict et al., 1998; Spreen and Strauss, 1998; Delis et al., 2000), employing language as a core construct and thus are not feasible to model using mice.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Kaplan et al., 1978
- Not checked yetcites Benedict et al., 1998 source
- Not checked yetcites Spreen and Strauss, 1998
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Other cognitive domains impaired in human AD such as those involving language (i.e., verbal acuity tasks and verbal recall tasks) simply cannot be modeled in rodent models.
In the paper
“Composite scores encompassing multiple neuropsychological tests are often used and can provide some of the most reliable assessments of global cognitive status relating to AD as well as serving as efficacy outcome measures in clinical trials (Bernick et al., 2012).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Cognitive neuropsychological assessment summary
What the sources say
- Not checked yetcites Bernick et al., 2012 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“These early deficits in episodic memory are followed closely by deficits in semantic memory, and both are developed before other deficits in cognitive domains such as attention, visuospatial memory, or executive function (Bondi et al., 2008).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Cognitive neuropsychological assessments used in the AD field > Cognitive neuropsychological assessment summary
What the sources say
- Not checked yetcites Bondi et al., 2008
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Perhaps the most widely employed spatial working memory task is that of the Morris Water Maze (MWM) (Morris et al., 1982).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Morris et al., 1982
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Other common tasks of murine spatial working memory are the Radial Arm Water Maze (RAWM) and the Barnes Maze (Barnes, 1979; Diamond et al., 1999; Alamed et al., 2006).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
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None of the sources cited for this claim have been checked yet.
In the paper
“Depending on the baiting paradigm, unimpaired rats and mice will quickly learn where the food reward is and which arms have previously been visited, and will avoid re-entering a previously entered arm.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling working memory
What the sources say
- Not checked yetcites Olton and Samuelson, 1976
- Not checked yetcites Olton et al., 1979
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Response inhibition is required for the appropriate control of an individual's behavioral actions in response to a stimulus (Robbins, 1996; Humby et al., 1999; Perry and Hodges, 1999; Romberg et al., 2013a).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling executive function
What the sources say
- Not checked yetcites Robbins, 1996
- Not checked yetcites Humby et al., 1999
- Not checked yetcites Perry and Hodges, 1999
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“In many ways, set-shifting tasks are similar to the Wisconsin Card Sorting Task in that they form the gold standard for assessing executive function (Drewe, 1974; Robinson et al., 1980; Arnett et al., 1994).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling executive function
What the sources say
- Not checked yetcites Drewe, 1974
- Not checked yetcites Robinson et al., 1980
- Not checked yetcites Arnett et al., 1994 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“All of the rodent behavioral tasks discussed in this section have been specifically developed to assess deficits in cognitive domains related to what is seen in human AD.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Summary of mouse behavioral tests
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Cognitive decline is a defining feature of AD, and many mouse models have been developed that recapitulate aspects of the cognitive impairments seen in AD (Elder et al., 2010; Hochgrafe et al., 2013; Platt et al., 2013).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
What the sources say
- Not checked yetcites Elder et al., 2010
- Not checked yetcites Hochgrafe et al., 2013
- Not checked yetcites Platt et al., 2013
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, caution should be used when attempting to correlate any preclinical finding concerning episodic memory in mice to that of human cognition.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence.
None of the sources cited for this claim have been checked yet.
In the paper
“However, work over the past few decades on episodic-like memory across a number of animal species has suggested otherwise, and several mouse behavioral tasks designed at assessing episodic-like memory have been developed (Clayton and Dickinson, 1998; Clayton et al., 2001; Griffiths and Clayton, 2001; Morris, 2001; Davis et al., 2013a,b).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
What the sources say
- Not checked yetcites Clayton and Dickinson, 1998
- Not checked yetcites Clayton et al., 2001
- Not checked yetcites Griffiths and Clayton, 2001
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“This is largely because the human tasks rely on language as a foundational construct for assessment. Obviously, there exists no such component in the WWWhich task for mice.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Historically, episodic memory was thought to be unique to humans (Tulving and Markowitsch, 1998).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
What the sources say
- Not checked yetcites Tulving and Markowitsch, 1998
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“While the NOR task itself is too simplistic a task to be considered a true episodic memory task (rather it is considered a task of recognition memory), the WWWhich task is able to model episodic-like memory.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling episodic memory
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Touchscreen versions of this task are also available in which the nose poke holes and stimulus lights are replaced with an LCD screen (Romberg et al., 2011; Bussey et al., 2012).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > How commonly used preclinical mouse behavioral tasks relate to the clinical neuropsychological assessment tests in human AD? > Modeling attention
What the sources say
- Not checked yetcites Romberg et al., 2011
- Not checked yetcites Bussey et al., 2012
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, the contributions of both background strain and likely overexpression of mutant human APP genes on brain development and function must always be considered with regard to observed cognitive deficits in the various AD mouse models.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although no one animal model fully replicates the progression of cognitive impairments seen in the human disease, AD mouse models have been invaluable in advancing our knowledge of the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Deficits in recognition memory appear to develop after the working memory deficits in this model, as the first reported deficits in the NOR task are at 6 months old (Dodart et al., 1999).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > PDAPP
What the sources say
- Not checked yetcites Dodart et al., 1999
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Each transgenic mouse model of AD provides different insights into aspects of AD pathogenesis and the cognitive deficits associated with the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“TgCRND8 are impaired on spatial working memory tasks starting at 3 months of age. These deficits are seen in the MWM and progress with age of the animal (Janus et al., 2000; Chishti et al., 2001; Gortz et al., 2008; Richter et al., 2008; Ambree et al., 2009).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > TgCRND8
What the sources say
- Not checked yetcites Janus et al., 2000
- Not checked yetcites Chishti et al., 2001
- Not checked yetcites Gortz et al., 2008
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The deficits appear to be progressive with age, and at 12 months old the animals also show cognitive deficits in a reference memory version of the Barnes maze (Prut et al., 2007).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP23
What the sources say
- Not checked yetcites Prut et al., 2007
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The cognitive deficits in recognition memory do not appear as robust as those in working memory in this model as there are inconsistent reports in the literature (Dodart et al., 1999, 2002; Chen et al., 2000).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > PDAPP
What the sources say
- Not checked yetcites Dodart et al., 1999, 2002
- Not checked yetcites Chen et al., 2000
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“It should be noted that most of the AD mouse models are representative of the familial form of AD (FAD) which accounts for only a small percentage of the total AD cases each year (Campion et al., 1999).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models
What the sources say
- Not checked yetcites Campion et al., 1999
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Impairments in reference memory develop by 6 months and persist through the rest of the life of this model (Reiserer et al., 2007; Bernardo et al., 2009; O'leary and Brown, 2009).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP/PS1
What the sources say
- Not checked yetcites Reiserer et al., 2007
- Not checked yetcites Bernardo et al., 2009 source
- Not checked yetcites O'leary and Brown, 2009
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Cognitive deficits are first seen at 3 months of age in the RAWM spatial working memory task and are also reported by 6 months of age in the MWM (Cao et al., 2007; Ding et al., 2008).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP/PS1
What the sources say
- Not checked yetcites Cao et al., 2007
- Not checked yetcites Ding et al., 2008
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“However, they do not appear to progress with the age of the animal and there has even been a report of no recognition memory deficits in old animals in advanced stages of the disease (Karl et al., 2012).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > J20
What the sources say
- Not checked yetcites Karl et al., 2012
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These working memory deficits are followed temporally with the development of associative learning impairment in fear conditioning (Ohno et al., 2006; Devi and Ohno, 2010) as well as the development of deficits in a working memory version of the Y-maze (Oakley et al., 2006; Devi and Ohno, 2012; Shukla et al., 2013).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > 5×FAD
What the sources say
- Not checked yetcites Ohno et al., 2006
- Not checked yetcites Devi and Ohno, 2010
- Not checked yetcites Oakley et al., 2006
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The APP/PS1 knock-in mouse model (first described in Flood et al., 2002) uses endogenous promoters to drive the expression of humanized amyloid beta sequence, and AD-like pathology and cognitive deficits develop in the absence of APP or PS1 overexpression (Flood et al., 2002).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP/PS1 KI
What the sources say
- Not checked yetcites Flood et al., 2002
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The first observable deficits in this model are shown in associative learning and present themselves between 4 and 5 months of age (Dineley et al., 2002).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP + PS1
What the sources say
- Not checked yetcites Dineley et al., 2002
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These deficits are followed by impairments in associative memory (appearing by 14 months of age Thibault et al., 2012) and in recognition memory (not developing until 15 months of age Webster et al., 2013).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of the cognitive deficits seen in the commonly used AD mouse models > APP/PS1 KI
What the sources say
- Not checked yetcites Thibault et al., 2012
- Not checked yetcites Webster et al., 2013
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Indeed, these non-cognitive symptoms are seen as a very important concern among the family members of the patients and caregivers alike (Tan et al., 2005).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models
What the sources say
- Not checked yetcites Tan et al., 2005
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Further, these disturbances increase with the age of the animals and with the severity of the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Locomotor activity
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These non-cognitive symptoms are often more difficult to deal with, as they compose important sources of distress and psychological burden on the family members/caregivers and can drastically affect the quality of life of patients by leading to institutionalization (Hope et al., 1998; Shin et al., 2005).”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models
What the sources say
- Not checked yetcites Hope et al., 1998
- Not checked yetcites Shin et al., 2005
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“This suggests that perhaps aggressive deficits correlate best with moderate to severe stages of the disease, which is also what is observed clinically in human AD”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Aggressive behaviors
What the sources say
- Not checked yetcites Senanarong et al., 2004
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Numerous meta-analysis studies have linked depression and AD”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Depressive symptoms
What the sources say
- Not checked yetcites Chen et al., 1999
- Not checked yetcites Charlson and Peterson, 2002
- Not checked yetcites Ownby et al., 2006
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“These disturbances are characterized by the AD patient's propensity to frequently awaken during the nighttime and to increase the amount of time slept during the day”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Temporal progression of AD-like non-cognitive behavioral abnormalities seen in the commonly used mouse models > Circadian rhythm and sleep disruptions
What the sources say
- Not checked yetcites Ancoli-Israel et al., 1989 source
- Not checked yetcites Okawa et al., 1991
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“AD is not just a memory disorder, rather it is a complex disease with many different non-cognitive neuropsychiatric symptoms which are an important source of distress and a psychological burden on family members and caregivers alike.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Conclusions
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“No one animal model fully replicates the pathogenesis of AD, but rather only model different aspects of the disease.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Conclusions
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the anatomical makeup and cognitive ability of mice make it difficult to model all of the intricacies of higher-order cognitive function exclusive to humans.”
§ Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models > Conclusions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper relies on this without support.
No animal model recapitulates the entirety of AD in humans.
“However, no animal model recapitulates the entirety of AD in humans, and therefore it is important to understand both the utility and limitations of particular animal models.”
The paper relies on this without support.
Outside of frontotemporal lobar degeneration (FTLD), one does not see widespread cortical NFTs without abundant plaque pathology.
“It should be noted that outside of frontotemporal lobar degeneration (FTLD), one does not see widespread cortical NFTs without abundant plaque pathology.”
The paper relies on this without support.
During late stages (Braak stage V–VI), NFTs increase in number and manifest in neocortical areas responsible for higher cognitive domains such as executive function, visuospatial capacities, and speech in synchrony with observed AD-related cognitive deficits in these respective cognitive domains.
“During the late stages (Braak stage V–VI), NFTs increase in number and manifest in neocortical areas responsible for higher cognitive domains such as executive function, visuospatial capacities, and speech in synchrony with observed AD-related cognitive deficits in these respective cognitive domains.”
The paper relies on this without support.
Some of the earliest neuropathological changes in AD are in the hippocampus and entorhinal cortex, followed by changes in the medial temporal lobe.
“Some of the earliest neuropathological changes in AD are in the hippocampus and entorhinal cortex, followed by changes in the medial temporal lobe.”
The paper relies on this without support.
Neuropsychological assessment is the most reliable means to clinically evaluate the cognitive deficits seen in humans.
“Neuropsychological assessment is the most reliable means to clinically evaluate the cognitive deficits seen in humans.”
The paper relies on this without support.
Other cognitive domains impaired in human AD such as those involving language (i.e., verbal acuity tasks and verbal recall tasks) simply cannot be modeled in rodent models.
“Other cognitive domains impaired in human AD such as those involving language (i.e., verbal acuity tasks and verbal recall tasks) simply cannot be modeled in rodent models.”
The paper relies on this without support.
Working memory is perhaps one of the most well modeled aspects of the memory deficits in AD.
“Working memory is perhaps one of the most well modeled aspects of the memory deficits in AD.”
The paper relies on this without support.
As the patient moves from the preclinical phase of AD into MCI, more cognitive domains begin to be affected.
“As the patient moves from the preclinical phase of AD into MCI, more cognitive domains begin to be affected.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In preclinical AD, mouse models that contain a mutation in amyloid precursor protein (APP) have been widely used as models of AD, which play an essential role in cognitive function (Webster et al., 2014).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Webster et al., 2014
Experimental — accuracy not yet measuredIn the citing paper
“There have been many clinicopathological studies that have correlated amyloid plaques with cognitive deficits in AD, with an emerging picture that the strongest correlation exists in the earliest stages of the disease and this association greatly weakens as NFTs and neocortical degeneration become more widespread [9, 102, 103, 157, 160, 169].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [169]
In the citing paper
“On the other hand, numerous studies have documented a strong link between neocortical NFTs and cognitive loss[26, 46, 48, 97, 123, 160, 169].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [169]
Citations
Cites
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The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment
Nasreddine, Z. S., Phillips, N. A., Bédirian, V., Charbonneau, S., Whitehead, V., Collin, I., Cummings, J. L., & Chertkow, H. (2005) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.2005.53221.x · Cited by 25,553
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657 · cited 1×
“Once the AD patient progresses past MCI and into dementia, general cognition continues to decline with deficits appearing in all respective cognitive domains (Huff et al., 1987; Locascio et al., 1995; Lambon Ralph et al., 2003; Mckhann et al., 2011).”
BackgroundPlace navigation impaired in rats with hippocampal lesions
Morris, R. G. M., Garrud, P., Rawlins, J. N. P., & O'Keefe, J. (1982) · Nature · doi:10.1038/297681a0 · Cited by 6,340 · cited 8×
“In this model, the cognitive deficits first present themselves in spatial working memory at 4 months of age when assessed by MWM testing (Hartman et al., 2005).”
MethodInfluentialKaplan, E., Goodglass, H., Weıntraub, S., & Segal, O. (2001) · Medical Entomology and Zoology · Cited by 4,378
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210 · cited 6×
“(Promoter: Hamster PrP Promoter, Symbol: Tg (APPSWE) 2576Kha, MGI ID: 2385631) In the Tg2576 mouse (Hsiao et al., 1996), the first presentation of cognitive deficits is seen at 5 months of age in spatial working memory (Arendash et al., 2004).”
BackgroundMethodInfluentialA new rating scale for Alzheimer's disease
(1984) · American Journal of Psychiatry · doi:10.1176/ajp.141.11.1356 · Cited by 4,175 · cited 1×
“The Alzheimer’s Disease Assessment Scale (ADAS) was specifically developed to measure the severity of symptoms commonly seen in AD (Rosen et al., 1984).”
MethodMoms, J. C., Heyman, A., Mohs, R. C., Hughes, J. P., van Belle, G., Fillenbaum, G., Mellits, E. D., & Clark, C. (1989) · Neurology · doi:10.1212/wnl.39.9.1159 · Cited by 4,130 · cited 1×
“…tests are extensively used as clinical diagnostic tools (Schmitt, 1994) as well as to track the progression of the disease (Flicker et al., 1984; Morris et al., 1989; Storandt and Hill, 1989; Storandt, 1991; Welsh et al., 1991, 1992; Locascio et al., 1995; Albert, 1996; Storandt et al., 1998;…”
MethodTriple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126 · cited 1×
“…2006), 25: (Ohno et al., 2006), 26: (Shukla et al., 2013), 27: (Devi and Ohno, 2010), 28:(Devi and Ohno, 2012), 29: (Urano and Tohda, 2010), 30: (Oddo et al., 2003), 31: (Clinton et al., 2007), 32: (Carroll et al., 2007), 33: (Gimenez-Llort et al., 2007), 34: (Billings et al., 2005), 35:…”
Blessed, G., Tomlinson, B. E., & Roth, M. (1968) · British Journal of Psychiatry · doi:10.1192/bjp.114.512.797 · Cited by 4,117 · cited 1×
“There have been numerous clinicopathological studies attempting to correlate amyloid plaques with the cognitive deficits seen in AD (Blessed et al., 1968; Tomlinson et al., 1970; Duyckaerts et al., 1990, 1998; Berg et al., 1998; Gold et al., 2000; Mungas et al., 2001; Tiraboschi et al., 2002, 2004;…”
Background
Flagged first, then by citations
Research works printed but not linked: 2
- Benedict, 1994, Preliminary standardization and validation of a multiple-form test for the assessment of visuospatial memory, Arch. Clin. Neuropsychol, 9, 109
- Benton, 1992, Benton Visual Retention Test, 5th Edn
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Items 501–600 of 752
Wang, H., Li, Q., Tang, H., Ding, J., Xu, N., Sun, S., & Chen, S. (2019) · Brain and Behavior · doi:10.1002/brb3.1316 · Cited by 7
Detection and Prediction of Mild Cognitive Impairment in Alzheimer’s Disease Mice
Rai, S. P., Bascuñana, P., Brackhan, M., Krohn, M., Möhle, L., Paarmann, K., & Pahnke, J. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200675 · Cited by 7
“However, an enormous heterogeneity has been observed between the time course and the progression of cognitive change across different AD mouse models [31].”
BackgroundClement, A., Pedersen, M. M., Stensballe, A., Wiborg, O., & Asuni, A. A. (2021) · Genes Brain & Behavior · doi:10.1111/gbb.12766 · Cited by 6
Lessons from a Rare Familial Dementia: Amyloid and Beyond
Cantlon, A., Frigerio, C. S., & Walsh, D. M. (2015) · Journal of Parkinson’s Disease and Alzheimer’s Disease · doi:10.13188/2376-922x.1000009 · Cited by 8
Qiu, N., Hou, H.-M., Guo, T.-Y., Lv, Y.-L., zhou, Y., Zhang, F., Zhang, F., Wang, X., Chen, W., Gao, Y., et al. (2024) · Neurochemical Research · doi:10.1007/s11064-024-04156-2 · Cited by 5
“Moreover, APP/ PS1/Tau triple transgenic (3 × Tg-AD) mice [16], as one of the closest available mouse models of human AD, which have multiple pathological features such as Aβ deposition and Tau protein phosphorylation, was used to explore the changes in the expression of PDE8A and PDE8B in the…”
Smith, T. M., Knudsen, K. J., & Ritchie, S. A. (2024) · Brain Research · doi:10.1016/j.brainres.2024.149132 · Cited by 7
“Most currently-available AD animal models are based on the production or incorporation of β -amyloid or tau through either mutation or injection (Puzzo et al., 2015; Webster et al., 2014).”
BackgroundMatsuura, Y., Ueda, M., Higaki, Y., Watanabe, K., Habara, S., Kamino, S., Saji, H., & Enomoto, S. (2016) · Nuclear Medicine and Biology · doi:10.1016/j.nucmedbio.2016.02.007 · Cited by 6
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. (2022) · Springer eBooks · doi:10.1007/978-3-031-15080-7_98 · Cited by 6
Jiang, L.-X., Huang, G.-D., Tian, Y., Cong, R., Meng, X. W., Wang, H., Zhang, C., & Yu, X. (2023) · BMC Biology · doi:10.1186/s12915-023-01674-3 · Cited by 7
“As the disease progresses, AD patients gradually develop impairments in episodic memory, semantic memory, working memory (WM), and visuospatial memory [8–11].”
BackgroundXin, Y., Chu, T., Zhou, S., & Xu, A. (2023) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2023.110821 · Cited by 6
“…including Morris water maze for episodic-like learning and memory (Hernandez-Mercado and Zepeda, 2021), Y maze for spatial working memory (Webster et al., 2014), novel object recognition for recognition memory (Lissner et al., 2021), radial arm maze for working memory (Zlomuzica and…”
MethodTemporal Alterations in White Matter in AnAppKnock-In Mouse Model of Alzheimer’s Disease
Morrissey, Z. D., Gao, J., Shetti, A., Li, W., Zhan, L., Li, W., Fortel, I., Saido, T. C., Saito, T., Ajilore, O., et al. (2024) · eNeuro · doi:10.1523/eneuro.0496-23.2024 · Cited by 8
“Despite the low prevalence of FAD, study of the genetics of these FAD patients has led to the development of many commonly used AD mouse models (Webster et al., 2014).”
BackgroundResultHayashi, M., Kudo, C., Hanamoto, H., Maegawa, H., Usami, N., & Niwa, H. (2024) · Physiology & Behavior · doi:10.1016/j.physbeh.2024.114652 · Cited by 6
Kour, D., Khajuria, P., Sharma, K., Sharma, A., Sharma, A., Ali, S. M., Wazir, P., Ramajayan, P., Sawant, S. D., Nandi, U., et al. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1525364 · Cited by 8
“Along with spatial memory, the decline in other behavior parameters is a common feature of AD (Albert, 1996; Pottorf et al., 2022; Webster et al., 2014).”
Duong, Q.-V., Kintzing, M. L., Kintzing, W. E., Abdallah, I. M., Brannen, A. D., & Kaddoumi, A. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20061489 · Cited by 6
“An APP/PS1 mouse model develops reference memory cognitive impairments at a later age (and at a temporally slower pace) than the 5xFAD model [41,42].”
Focused Transcranial Ultrasound for Treatment of Neurodegenerative Dementia
Nicodemus, N., Becerra, S. A., Kuhn Taylor, P., Packham, H., John, D. E. G., Mahdavi, K. D., Iovine, J., Santosh, K., Pereles, S., Whitney, M., et al. (2019) · Journal of Neurodegenerative Disorders · doi:10.36959/459/599 · Cited by 6
Lee, J. H., Ştefan, S., Walek, K. W., Nie, J., Min, K., Yang, T.-S., & Lee, J. (2023) · Biomedical Optics Express · doi:10.1364/boe.481826 · Cited by 6
Klimenko, M. O., Mishchenko, T. A., Mitaeva, Y. I., Kondakova, E. V., Mitroshina, Е. V., & Vedunova, M. V. (2023) · Neurology International · doi:10.3390/neurolint15030049 · Cited by 6
“The use of 5xFAD transgenic mice allows the modeling of a familial form of AD characterized by the formation of amyloid plaques in the brain [14,15].”
BackgroundBalu, D., Valencia‐Olvera, A. C., Deshpande, A., Narayanam, S., Konasani, S., Pattisapu, S., York, J. M., Thatcher, G. R. J., LaDu, M. J., & Tai, L. M. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1374825 · Cited by 6
“In FAD transgenic mouse models, including EFAD mice, learning and memory de fi cits are often assessed using the Morris water maze test (31, 32, 50, 51).”
MethodLearning Deficits in Adult Mitochondria Carrier Homolog 2 Forebrain Knockout Mouse
Aloni, E., Ruggiero, A., Gross, A., & Segal, M. (2018) · Neuroscience · doi:10.1016/j.neuroscience.2018.10.035 · Cited by 6
Identification of highest neurotoxic amyloid-β plaque type showing reduced contact with astrocytes
Mitsubori, M., Takeda, K., Nagashima, S., Ishido, S., Matsuoka, M., Inatome, R., & Yanagi, S. (2021) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2021.02.081 · Cited by 6
Home cage measures of Alzheimer's disease in the rTg4510 mouse model
Barabas, A. J., Robbins, L., & Gaskill, B. N. (2022) · Genes Brain & Behavior · doi:10.1111/gbb.12795 · Cited by 5
“animal models of AD are typically assessed for spatial memory deficits using the Morris Water Maze (MWM).(5) Originally designed for rats, the MWM is used in both rat and mouse models.”
MethodSolving the Puzzle of Neurodegeneration
Wolfe, M. S. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811304-2.00001-8 · Cited by 6
Liang, Y., Sun, Z., Chiu, K., & Hu, Y. S. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e39353 · Cited by 5
Chen, T., Chen, Y., Hsu, M.-L., Liao, Y. J., Wu, C.-H., Yao, C., Yang, W., Lin, W., & Lin, Y. (2024) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.4c07659 · Cited by 5
Babygirija, R., Green, C. L., Sonsalla, M. M., Le, I. M. F., Xiao, F., Yandell, S., Calubag, M. F., Trautman, M. E., Tobon, A., Matoska, R., et al. (2026) · Advanced Science · doi:10.1002/advs.202515220 · Cited by 7
Wang, X., Huang, R., Huang, B., & Li, X. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230533 · Cited by 5
“APP/PS1 transgenic mice were used as AD models [19], and animal experiments were divided into the WT group (wild-type C57BL/6 mice), APP/PS1 model group (APP/PS1 transgenic mice), APP/PS1 + sh-NC group (APP/PS1 mice injected sh-NC), and APP/PS1 + sh-S1PR2 group (APP/PS1 mice injected sh-S1PR2),…”
Unraveling Alzheimer’s: Exploring the Gut Microbiota–Brain Axis as a New Frontier in Understanding
Rashid, S. M., Razak, R., Tantray, A. K., James, A. W., Showkat, N., Shehjar, F., Jan, F., Ahmad, S. B., Khan, A., & Shah, Z. A. (2024) · Journal of dementia and Alzheimer's disease · doi:10.3390/jdad1010003 · Cited by 5
“Based on clinical and preclinical studies, the production of some biomolecules, like neuromodulators and neurotransmitters, from GM has a direct impact on gut–brain communication, behavioral changes and brain activities [31–34].”
BackgroundLiu, F.-W., Liu, Y., Shen, X.-R., Du, J., Zhang, H., & Hou, X. (2024) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2024.1391082 · Cited by 5
Olanzapine enhances early brain maturation through activation of the NODAL/FOXH1 axis
Teng, Z., Chen, Z., Zou, T., Su, Y., Zeng, H., Sun, S., Chen, H., Liu, J., Qin, Y., Wu, H., et al. (2024) · iScience · doi:10.1016/j.isci.2024.110917 · Cited by 5
Liang, C., Okamoto, A. A., Karim, F., Kawauchi, S., Melkonyan, L., Danh, T. B., & Mukherjee, J. (2025) · NeuroImage · doi:10.1016/j.neuroimage.2025.121092 · Cited by 5
“Transgenic mice models allow the study of specific pathologies such as A β plaques and neurofibrillary tangles (NFT, tau) in AD (Webster et al., 2014).”
Patterns of cognitive decline and somatosensory processing in a mouse model of amyloid accumulation
Uddin, O., Arakawa, K., Raver, C., Garagusi, B., & Keller, A. (2021) · Neurobiology of Pain · doi:10.1016/j.ynpai.2021.100076 · Cited by 6
Fan, S., Li, L., Liu, L., Li, H., Xian, X., & Li, W. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.905403 · Cited by 5
“The model exhibits pathological manifestations consistent with AD (Webster et al., 2014).”
BackgroundHuman Brain Banking as a Convergence Platform of Neuroscience and Neuropsychiatric Research
Liu, F., Yin, X., Cong, C., Wang, Y., & Ma, C. (2022) · Human Brain · doi:10.37819/hb.001.001.0204 · Cited by 5
“Over the years, Tg animal models and cell research have overshadowed human tissues, especially brain or other nerve tissues (Duyckaerts et al., 2008; Webster et al., 2014).”
BackgroundYeh, C.-M., Sun, Y.-Y., Chen, T., Hung, Y., Lee, G.-C., Yang, W., & Lin, Y. (2023) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.3c00157 · Cited by 5
Wang, Y., Xiao, Z., Yin, H., Ren, Z., Ma, X., Wang, Y., Zhang, Y., Fu, X., Zhang, F., & Zeng, L. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e37589 · Cited by 5
“The experimental environment was cleaned thoroughly after each trial [32].”
MethodMartínez-Drudis, L., Bérard, M., Musiol, D., Rivest, S., & Oueslati, A. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e39571 · Cited by 6
Karsuntseva, E. K., Voronova, A. D., Andretsova, S. S., Shishkina, V. S., Chadin, A. V., Fursa, G. A., Fedorov, A. V., Reshetov, I. V., Stepanova, O. V., & Chekhonin, V. P. (2024) · Bulletin of Experimental Biology and Medicine · doi:10.1007/s10517-024-06293-8 · Cited by 5
“The model was validated in Y-maze, passive avoidance, and Morris water maze tests that reveal changes in cognitive abilities (spatial orientation, exploration of new space, memory and learning abilities) in experimental animals [25,26].”
Brewer, K. L., Tran, T. D., & Meggs, W. J. (2015) · Journal of Medical Toxicology · doi:10.1007/s13181-015-0480-1 · Cited by 5
“This task was first developed to assess hippocampal-based spatial navigation learning in rats [21] and is now widely adopted for rodent models of traumatic brain injury [22] and neurodegenerative disorders [23].”
MethodAcute stressors do not impair short-term memory or attention in an aged mouse model of amyloidosis
DiMarco, G. M., Harris, B. N., Savonenko, A. V., & Soto, P. L. (2023) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2023.1151833 · Cited by 6
“, 2001), which has been used in a variety of behavioral paradigms such as the Morris Water Maze (MWM), Novel Object Recognition (NOR) task, and operant tasks (Arendash et al., 2001; Savonenko et al., 2003, 2005; Jankowsky et al., 2004; Cao et al., 2007; Cheng et al., 2014; Webster et al., 2014; Harris et al., 2023; So…”
BackgroundMethodXu, M. Q., Liu, J., Liu, Q., Gong, Y., Li, Y., Zhang, J., Shi, S., & Shi, Y. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1326394 · Cited by 5
Xing, X., Sha, S., Chen, X.-H., Guo, W., Guo, R., Jiang, T., & Cao, Y. (2015) · Neurochemical Research · doi:10.1007/s11064-015-1559-4 · Cited by 5
“Impairments in associative learning were described in fear conditioning tasks starting at 6–8 months of age, and passive avoidance deficits have also been described at 12 months of age [20].”
Protective Effect of Wheat Bran Extract against β-Amyloid-induced Cell Death and Memory Impairment
Lee, C., Park, G.-H., Lee, J.-W., & Jang, J. (2015) · The Korea Journal of Herbology · doi:10.6116/kjh.2015.30.1.67 · Cited by 5
Gautam, A. S., Akhtar, M. Z., Lasure, V., Kumari, N., Pandey, S. K., Dey, M., & Singh, R. K. (2025) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-025-10246-x · Cited by 4
“However, these 2014; Webster et al. 2014).”
Li, H., Hua, Q., Cheng, S., Liu, X., Cai, Q., Zhang, J., Peng, T., Li, J., Wang, C., Liang, C., et al. (2024) · Combinatorial Chemistry & High Throughput Screening · doi:10.2174/0113862073311518240416070410 · Cited by 4
Tang, S., Luo, W., Cheng, C., Shen, L., Wu, X., & Xiao, X. (2025) · Biochemistry and Biophysics Reports · doi:10.1016/j.bbrep.2025.102089 · Cited by 4
Rutsch, A., Iachizzi, M., Kirundi, J., Kantsjö, J. B., Planchette, A., Müller, T., Schmitz, W., Rađenović, A., Doenlen, R., de Agüero, M. G., et al. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.106084 · Cited by 4
“We have introduced tests to assess different aspects of learning and memory 21 in mice, such as short-and long-term memory, anxiety and exploration, learning and recognition while maintaining their hygiene status, in sterile flexible film isolators, allowing for longitudinal studies in the same…”
Smith, A. S., Gossman, K. R., Dykstra, B., Gao, F. P., & Moskovitz, J. (2022) · Antioxidants · doi:10.3390/antiox11040775 · Cited by 4
“The Y-maze test is a simple and common maze used to assess spatial working memory in mice by measuring their willingness to explore new environments [25].”
MethodAnimal Model for Alzheimer’s Disease, Parkinson’s Disease, and Schizophrenia
Sivaraman, D., Arunadevi, R., Nandan, M., Chandrababu, K., Chakrapani, P. S. B., & Sivan, U. (2024) · Springer eBooks · doi:10.1007/978-981-97-0048-6_11 · Cited by 4
Gladen-Kolarsky, N., Neff, C. J., Hack, W. R., Brandes, M. S., Wiedrick, J. T., Meza‐Romero, R., Lockwood, D. R., Quinn, J. F., Offner, H., Vandenbark, A. A., et al. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-024-01433-5 · Cited by 4
“The NORT, one of the best known tests for assessing associative recognition memory (Webster et al. 2014 ; Padua et al. 2024 ), was used in these experiments.”
Lu, H., Liu, S., Zhang, S., Chen, J., & Chen, Q. (2025) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2025.141048 · Cited by 4
Bergamini, G., Massinet, H., Durkin, S., & Steiner, M. A. (2022) · Physiology & Behavior · doi:10.1016/j.physbeh.2022.113787 · Cited by 4
Blackwell, A. A., Jodelka, F. M., Lake, R. I., Hastings, M. L., & Wallace, D. G. (2022) · Neuroscience · doi:10.1016/j.neuroscience.2022.12.012 · Cited by 6
“Most of the work assessing spatial orientation in patients and rodent models of AD have focused on the use of visual environmental information to guide movement (Henderson et al., 1989; Tetewsky and Duffy, 1999; Duffy et al., 2004; Possin, 2010; Webster et al., 2014; Tuena et al., 2021).”
BackgroundWilliams, E., Mutlu-Smith, M., Alex, A., Chin, X. W., Spires‐Jones, T. L., & Wang, S. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221185 · Cited by 5
Wang, M., Wei, T., Yu, C., Li, R., Yin, Y., Yang, H.-C., Di, R., Xia, X., Qin, Q., & Tang, Y. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03840-8 · Cited by 6
“APP/PS1 mice are the most commonly used animal model for the study of AD, which first develops cognitive deficits at 3 months of age and Aβ deposits form in the brain at 6 to 7 months of age [21].”
Prospects and Challenges for Alzheimer Therapeutics
Wolfe, M. S. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-802173-6.00023-x · Cited by 5
Matsuura, Y., Ueda, M., Higaki, Y., Sano, K., Saji, H., & Enomoto, S. (2018) · Molecular Imaging and Biology · doi:10.1007/s11307-018-1253-4 · Cited by 4
Nackenoff, A. G., Hohman, T. J., Neuner, S. M., Akers, C. S., Weitzel, N. C., Shostak, A., Ferguson, S. M., Bennett, D. A., Schneider, J. A., Jefferson, A. L., et al. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/746222 · Cited by 4
Effect of Artesunate on Behavioral Functions in Experimental Model of Alzheimer’s Disease
Pattanayak, C., Patanaik, S. K., Srivastava, V., Das, M. C., & Sarkar, S. (2025) · Medical Journal of Dr D Y Patil Vidyapeeth · doi:10.4103/mjdrdypu.mjdrdypu_355_23 · Cited by 3
Wnuk, H. K., Orden, K. A. V., & Wang, K. H. (2025) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2025.106451 · Cited by 5
Huan, S., Yang, Y., Wang, D., Zhao, Y., Xiu, Z., & Zheng, Y. (2023) · Psychopharmacology · doi:10.1007/s00213-023-06393-9 · Cited by 3
A New Approach for Exploring Reperfusion Brain Damage in Hypoxic Ischemic Encephalopathy
Zhang, T., Zhang, Z., Geng, J., Lin, K., Lin, X., Jiao, M., Zhu, J., Guo, X., & Lin, Z. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03645-9 · Cited by 3
“The SAB of Y-maze test could be used to evaluate the learning and memory abilities of neonatal rodents [14].”
Vázquez-Durán, D. L., Ortega, A., & Rodríguez, A. (2024) · Molecular Neurobiology · doi:10.1007/s12035-024-03966-3 · Cited by 4
“Among the most widely used, we found mice that reproduce the characteristics of familial AD [78, 79], with mutations in presenilin 1 and 2 (PS1 and PS2) genes in APP and/or in TAU-related genes, such as MAPT.”
Liu, H.-X., Yu, C., & Qin, C. (2024) · Anais da Academia Brasileira de Ciências · doi:10.1590/0001-3765202420240120 · Cited by 3
The US9-Derived Protein gPTB9TM Modulates APP Processing Without Targeting Secretase Activities
Brandimarti, R., Irollo, E., & Meucci, O. (2022) · Molecular Neurobiology · doi:10.1007/s12035-022-03153-2 · Cited by 4
“Therefore, the expression of APPsw provides a well-established strategy to reproduce the amyloidogenic pathway in cellular and animal models [57].”
BackgroundValidity and value of metabolic connectivity in mouse models of β-amyloid and tauopathy
Ruch, F., Gnörich, J. S., Wind-Mark, K., Koehler, M., Zatcepin, A., Wiedemann, T., Gildehaus, F., Lindner, S., Boening, G., von Ungern‐Sternberg, B., et al. (2024) · NeuroImage · doi:10.1016/j.neuroimage.2024.120513 · Cited by 5
“…a significant increase in hippocampal regions in the conventional VOI-based analysis, being completely contradictory to the significant loss of spatial learning functions we detected in the MWM at approximately 15 months of age, also confirmed by other behavioral studies (Webster et al., 2014).”
ResultChen, P., Yao, C., Chien, P., Tsai, H.-J., Chen, Y., Chuang, J.-H., Chou, P.-L., Lee, G.-C., Lin, W., & Lin, Y. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.3c00633 · Cited by 3
Mottolese, N., Coiffard, O., Ferraguto, C., Manolis, A., Ciani, E., & Pietropaolo, S. (2024) · Autism Research · doi:10.1002/aur.3226 · Cited by 4
“…and ASD (e.g., (Kat et al., 2022; Lemaire-Mayo et al., 2020; Piquemal et al., 2020)) and they are often employed as the “ young ” control group in preclinical studies on aging and Alzheimer disease (e.g., (Bach et al., 1999; Pietropaolo et al., 2008; Radulescu et al., 2021; Webster et al., 2014)).”
γ-Secretase modulation and plaque regression in Alzheimer’s disease
Ghosh, S., Bhaskar, R., Singh, D. K. K., & Sinha, J. K. (2025) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/j.jpet.2025.103687 · Cited by 3
Wet or dry: translatable “water mazes” for mice and humans
Higa, K. K., Young, J. W., & Geyer, M. A. (2016) · Journal of Clinical Investigation · doi:10.1172/jci86071 · Cited by 3
Genetics and Genomic Basis of Sleep in Rodents
O’Hara, B. F., Jiang, P., Turek, F. W., & Franken, P. (2016) · Elsevier eBooks · doi:10.1016/b978-0-323-24288-2.00029-5 · Cited by 3
Glutamate Signalling in Object Novelty Recognition Memory Tests
Argyrousi, E. K., Heckman, P. R. A., & Prickaerts, J. (2018) · Handbook of behavioral neuroscience · doi:10.1016/b978-0-12-812012-5.00035-5 · Cited by 3
Roberson, E. D., & Kao, A. W. (2016) · Cambridge University Press eBooks · doi:10.1017/9781139924771.007 · Cited by 3
Spicer, M. M., Yang, J., Fu, D., DeVore, A. N., Lauffer, M. C., Atasoy, N. S., Atasoy, D., & Fisher, R. A. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.04.17.537272 · Cited by 3
“202 Working memory is one of the most well-modeled memory deficits in AD, and the most 203 widely used paradigms in mice are maze-tasks which require spatial working memory to solve 204 (61).”
Targeting SPI1 to mitigate amyloid-β pathology in Alzheimer's disease
Shao, J., Youngblood, H. A., & Yang, L. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251316593 · Cited by 3
“8,9 Additionally, future studies could also attempt to validate the role and mechanism of SPI1 in human AD patient samples.”
Luo, Z., Guo, J.-S., Pang, S., Wei, D., Ma, J., Zhang, L., Qi, X.-L., Guan, F., Gao, S., Gao, X., et al. (2024) · Acta Pharmacologica Sinica · doi:10.1038/s41401-024-01362-0 · Cited by 2
miR-449a mediated repression of the cell cycle machinery prevents neuronal apoptosis
Chauhan, M., Singh, K., Chongtham, C., Aneeshkumar, A. G., & Sharma, P. (2024) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2024.107698 · Cited by 3
“Various transgenic models for AD like APP/PS1 mice have been reported to exhibit cognitive defects re fl ected by impaired learning and memory (87, 88, 117), which is why they have served as a very useful model for studying AD pathology as well as developing anti-AD therapeutics (118 – 122).”
Sharing the spotlight: Uncovering common attentional dynamics across species
Glukhova, M., Tlaie, A., Taylor, R. T., Ferracci, P.-A., Shapcott, K. A., Mert, B., Arne, O., Ciuparu, A., Muresan, R. C., Havenith, M. N., et al. (2026) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1014191 · Cited by 2
Sun, R., Zimbalski, L.-K., Schreyer, S., Baidoe‐Ansah, D., Harutyunyan, A., Heuser, A., Lippert, R. N., Spranger, J., Mai, K., & Brachs, S. (2025) · Biology of Sex Differences · doi:10.1186/s13293-025-00737-0 · Cited by 2
“In APP23, the first onset of cognitive deficits begins at 3 months of age [22].”
Active immunization: A novel therapeutic strategy for treating Alzheimer's disease
Mazahir, F. (2025) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2025.178288 · Cited by 3
Xie, K., Ryan, D. P., Schröder, S., Freund, L. J., Bonn, S., Zhou, Y., & Ehninger, D. (2026) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03682-2 · Cited by 2
“Commonly used AD mouse models exhibit progressive Aβ accumulation, cognitive deficits, and neuroinflammation, reproducing key features of human AD [26–30].”
Spatial navigation and Alzheimer's disease
Berkowitz, L. E., Harvey, R. E., & Clark, B. J. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-815868-5.00043-8 · Cited by 2
Sporadic Alzheimer’s disease animal model using streptozotocin and APP/PS1 mice
Kelliny, S., Deng, I. B., Zhou, X., & Bobrovskaya, L. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-89833-1.00026-4 · Cited by 2
Deng, Z., Lee, A., Lin, T., Taneja, S., Kowdley, D., Leung, J. H., Hill, M., Tao, T., Fitzgerald, J., Yu, L., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252111689 · Cited by 2
“We followed the protocol developed for a mouse model of type 2 diabetes [25]; however, the decision to extend the study to 17 weeks was based on previous work by others [31,91] who described a slow, progressive amyloid plaque formation without significant cognitive decline in these mice.”
MethodGenetic and molecular basis of neurodegenerative diseases
Yogi, S., Sangeeth, A., Chimata, A. V., Padma, R., & Singh, A. K. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-23826-0.00002-7 · Cited by 2
Rocking during sleep reduces motor deficits and beta-amyloid levels in an Alzheimer’s mouse model
Zhang, L., Santoni, L., Ngo, N. A., Simayi, R., Ficiarà, E., de Vivo, L., & Bellesi, M. (2025) · iScience · doi:10.1016/j.isci.2025.112036 · Cited by 2
Murakami, S., & Halperin, A. S. (2014) · Frontiers in Genetics · doi:10.3389/fgene.2014.00269 · Cited by 2
“Importantly, motor activities are not always defective in AD but are abnormal (Webster et al., 2014).”
BackgroundBeker, S., Kellner, V., Chechik, G., & Stern, E. A. (2016) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2016.01.002 · Cited by 2
“Although the vast majority of AD mouse models report the first cognitive deficits at 6 months of age at the earliest [15], we show that most cells of APP/PS1 Tg(1) mice can be automatically detected at 2–4 months of age, before any behavioral sign of the disease occurs, and before the pathological hallmarks appear in…”
Genotype and Sex Differences in Longevity in Transgenic Mouse Models of Alzheimer’s Disease
Brown, R. E., Shin, S., Woodland, N., & Rae, E. A. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811353-0.00042-7 · Cited by 2
The effect of miR-101 on the memory of rats with a model of Alzheimer’s disease
Берченко, О. Г., Левічева, Н. О., Bevziuk, D., & Sokolik, V. V. (2020) · Regulatory Mechanisms in Biosystems · doi:10.15421/022054 · Cited by 2
“, 2015) and spatial orientation (spatial memory) (Mugantseva, 2010; Webster et al., 2014).”
BackgroundMethodInfluentialAnalysis of Biological Data by Graph Theory Approach Searching of Iron in Biological Cells
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Sleat, D. E., Maita, I., Banach-Petrosky, W. A., Larrimore, K. E., Liu, T. T., Cruz, D. L., Baker, L., Maxfield, F. R., Samuels, B. A., & Lobel, P. (2022) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2022.06.012 · Cited by 2
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In Vivo Assays for Amyloid-Related Diseases
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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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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