Evidence map›Paper›PMID 34074018›Full record

ReviewInternational journal of molecular sciences2021

Alzheimer's Disease Animal Models: Elucidation of Biomarkers and Therapeutic Approaches for Cognitive Impairment.

Tsuyoshi Nakai, Kiyofumi Yamada, Hiroyuki Mizoguchi

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

28 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Tsuyoshi NakaiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
Kiyofumi YamadaDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
Hiroyuki MizoguchiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.

Funding

biomedical research from the SRF, Japan nonGrants-in-Aid for Scientific Research from MEXT 19H03532, 19H05017, 19K21811, 20H01037the Hori Sciences and Arts Foundation nonthe Mishima Kaiun Memorial Foundation nonthe Strategic Research Program for Brain Science from the Japan Agency for Medical Research and Development (AMED) nonthe Takeda Science Foundation non
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-related and progressive neurodegenerative disorder. It is widely accepted that AD is mainly caused by the accumulation of extracellular amyloid β (Aβ) and intracellular neurofibrillary tau tangles. Aβ begins to accumulate years before the onset of cognitive impairment, suggesting that the benefit of currently available interventions would be greater if they were initiated in the early phases of AD. To understand the mechanisms of AD pathogenesis, various transgenic mouse models with an accelerated accumulation of Aβ and tau tangles have been developed. However, none of these models exhibit all pathologies present in human AD. To overcome these undesirable phenotypes,

Indexed as

Disease Models, AnimalAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBiomarkersCognitive DysfunctionGene Knock-In TechniquesMiceMice, Transgenictau ProteinsAmyloid beta-Protein PrecursorBiomarkerstau ProteinsAlzheimer’s diseaseamyloid cascade hypothesisanimal modelsbiomarkersneurofibrillary tanglespharmacological interventiontau

Identifiers

PMID34074018
PMCPMC8197360

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.