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Record W4404481502 · doi:10.26685/urncst.723

The Role of Synaptopathy in Alzheimer's Disease: A Review of Key Transgenic Mouse Models

2024· review· en· W4404481502 on OpenAlexaff
Hena Ahmad, Teresa I. Ng

Bibliographic record

VenueUndergraduate Research in Natural and Clinical Science and Technology (URNCST) Journal · 2024
Typereview
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicPluripotent Stem Cells Research
Canadian institutionsUniversity of Toronto
Fundersnot available
KeywordsGenetically modified mouseKey (lock)NeuroscienceTransgeneDiseaseBiologyMedicinePathologyGeneGeneticsEcology

Abstract

fetched live from OpenAlex

Introduction: Long-term potentiation (LTP) and its counterpart, long-term depression (LTD), are considered the cellular basis underpinning learning and memory. Impairments in these processes are associated with neurodegenerative diseases such as Alzheimer’s disease (AD). These impairments are emergent during the onset of AD, suggesting a critical role in the pathophysiology of AD. Popular transgenic AD models, such as 5xFAD, 3xTg, Tau MAPT P301L, and APPswe/PSEN1dE9 demonstrate changes in synaptic plasticity early during their lifespan. This systematic review aims to investigate localization and onset of synaptopathy associated with AD. Methods: A comprehensive literature search was conducted using PubMed (Medline) to identify common features across models associated with synaptic plasticity. Papers were screened through two stages. The first stage involved establishing a set of criteria, including search terms. The second stage centered on ensuring chosen studies focused on synaptopathy and utilized the models selected. Results: Eight studies were selected across the four transgenic mouse models that established onset and localization of synaptopathy in AD pathophysiology. In the majority of studies, impairments in synaptic plasticity were first found in the CA1 region of the hippocampus. Moreover, onset of these impairments developed prior to onset of neuropathology and behavioral or cognitive deficits. Impairments in synaptic plasticity included inhibition of glutamate release, decreased cell excitability, dendritic atrophy and impaired receptor signaling. Discussion: The results of this review suggest localization of synaptic plasticity impairments to the CA1 region preceding development of neuropathologies such as amyloid or tau aggregation and cognitive deficits. This indicates an early and critical role of synaptopathy at the CA1 region, implicating it as a potential causal factor in the pathophysiology of AD. Conclusion: While the FAD models evaluated in this review implicate changes in synaptic plasticity within AD, they are not representative of late onset AD (LOAD), the prevalent form of the disease in the population. Currently research using LOAD models is limited, causing reliance on FAD models for the study of AD. As prevalence of AD increases in the population, it is essential that new models of LOAD are developed and studied to further current understandings of AD pathophysiology.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.003
metaresearch head score (Gemma)0.004
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Not applicable · Consensus signal: none
GenreCandidate signal: Review · Consensus signal: Review
Teacher disagreement score0.014
Threshold uncertainty score0.014

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0030.004
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0030.002
Bibliometrics0.0140.011
Science and technology studies0.0000.001
Scholarly communication0.0010.002
Open science0.0020.001
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0030.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.066
GPT teacher head0.425
Teacher spread0.360 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designNot applicable
Domainnot available
GenreReview

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2024
Admission routes1
Has abstractyes

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