Evidence map›Paper›PMID 32317913›Full record

ReviewFrontiers in neuroscience2020

Hippocampal Deficits in Amyloid-β-Related Rodent Models of Alzheimer's Disease.

Yukti Vyas, Johanna M Montgomery, Juliette E Cheyne

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 67 citations in OpenAlex.

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  16. Serial reversal learning in an olfactory discrimination task in 3xTg-AD mice.Learning & memory (Cold Spring Harbor, N.Y.) · 2023
    Article
  17. Systematic characterization of a non-transgenic AβBiology of sex differences · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Yukti VyasDepartment of Physiology, Centre for Brain Research, University of Auckland, Auckland, New Zealand.
Johanna M MontgomeryDepartment of Physiology, Centre for Brain Research, University of Auckland, Auckland, New Zealand.
Juliette E CheyneDepartment of Physiology, Centre for Brain Research, University of Auckland, Auckland, New Zealand.
University of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease that is the most common cause of dementia. Symptoms of AD include memory loss, disorientation, mood and behavior changes, confusion, unfounded suspicions, and eventually, difficulty speaking, swallowing, and walking. These symptoms are caused by neuronal degeneration and cell loss that begins in the hippocampus, and later in disease progression spreading to the rest of the brain. While there are some medications that alleviate initial symptoms, there are currently no treatments that stop disease progression. Hippocampal deficits in amyloid-β-related rodent models of AD have revealed synaptic, behavioral and circuit-level defects. These changes in synaptic function, plasticity, neuronal excitability, brain connectivity, and excitation/inhibition imbalance all have profound effects on circuit function, which in turn could exacerbate disease progression. Despite, the wealth of studies on AD pathology we don't yet have a complete understanding of hippocampal deficits in AD. With the increasing development of

Indexed as

Alzheheimer’s diseasecircuit changeshippocampusmouse modelssynaptic plasticity

Identifiers

PMID32317913
PMCPMC7154147
OpenAlexW3015745164

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.