Cited by 222Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Rodent models for Alzheimer’s disease drug discovery

Open access
Puzzo, Daniela, Gulisano, Walter, Palmeri, Agostino, Arancio, Ottavio·2015·Expert Opinion on Drug Discovery

Abstract

INTRODUCTION: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by memory loss and personality changes, leading to dementia. Histopathological hallmarks are represented by aggregates of beta-amyloid peptide (Aβ) in senile plaques and deposition of hyperphosphorylated tau protein in neurofibrillary tangles in the brain. Rare forms of early onset familial Alzheimer's disease are due to gene mutations. This has prompted researchers to develop genetically modified animals that could recapitulate the main features of the disease. The use of these models is complemented by non-genetically modified animals. AREAS COVERED: This review summarizes the characteristics of the most used transgenic (Tg) and non-Tg models of AD. The authors have focused on models mainly used in their laboratories including amyloid precursor protein (APP) Tg2576, APP/presenilin 1, 3xAD, single h-Tau, non-Tg mice treated with acute injections of Aβ or tau, and models of physiological aging. EXPERT OPINION: Animal models of disease might be very useful for studying the pathophysiology of the disease and for testing new therapeutics in preclinical studies but they do not reproduce the entire clinical features of human AD. When selecting a model, researchers should consider the various factors that might influence the phenotype. They should also consider the timing of testing/treating animals since the age at which each model develops certain aspects of the AD pathology varies.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1517/17460441.2015.1041913

Cites

89 of 89 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Human brain organoids can fully replicate human biology and potentially reduce translational barriers from experimental findings to therapeutic applications.

    “Meanwhile, being entirely derived from human cells, these organoids can fully replicate human biology and potentially reduce the translational barriers from experimental findings to therapeutic applications (20–22), offering advantages over animal models (23–25).”

    From Understanding monocyte-driven neuroinflammation in Alzheimer’s disease using human cortical organoid microphysiological systems (2025) · cites this paper as [23]

    The Expert opinion section (page unavailable) says animal models reproduce only some aspects of Alzheimer’s disease and cannot recapitulate the entire human clinical picture. That supports the comparison with animal models, but the paper does not address whether human brain organoids fully replicate human biology or reduce translational barriers. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

2 of the 91 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Puzzo, D., Gulisano, W., Palmeri, A., & Arancio, O.
Affiliations
  • University of Catania (IT)
  • Columbia University (US)
Venue
Expert Opinion on Drug Discovery
Published
2015-04-30
Volume
10
Issue
7
Pages
703-711
ISSN
  • 1746-0441 (ISSN-L)
  • 1746-045X
OpenAlex
W1963514255
Cited by
222
References
91
Citations by year
2026: 11 · 2025: 18 · 2024: 13 · 2023: 24 · 2022: 19 · 2021: 25 · 2020: 16 · 2019: 19 · 2018: 30 · 2017: 22 · 2016: 22 · 2015: 3
FWCI
3.16
Type
journal article
Language
en
Open access
Locations
  • Expert Opinion on Drug Discovery (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG034248, AG034248)
  • National Institute of Neurological Disorders and Stroke (R01NS049442, NS49442)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, animal models, transgenic mice, APP/PS1 double transgenic mice, amyloid-beta, tau protein, amyloid plaques, neurofibrillary tangles, presenilin 1, amyloid precursor protein, physiological aging, drug discovery, preclinical testing
MeSH terms
Aging, Alzheimer Disease, Animals, Disease Models, Animal, Drug Evaluation, Preclinical, Humans, Mice, Transgenic, Rodentia, Species Specificity, Mice, Drug Discovery

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.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review