Evidence map›Paper›PMID 35887075›Full record

ReviewInternational journal of molecular sciences2022

The Role of Neurotrophin Signaling in Age-Related Cognitive Decline and Cognitive Diseases.

Tadahiro Numakawa, Haruki Odaka

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.7field-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

46 citing papers in PubMed, 62 citations in OpenAlex.

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  15. Extracellular vesicles and circulating nucleic acids · 2026
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  18. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
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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

2 authors at 2 institutions in 1 country.

Tadahiro NumakawaDepartment of Cell Modulation, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Haruki OdakaCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Central 6, Tsukuba 305-8566, Japan.
Kumamoto University · JPNational Institute of Advanced Industrial Science and Technology · JP

Funding

Japan Society for the Promotion of Science JSPS KAKENHI 19K16263Japan Society for the Promotion of Science JSPS KAKENHI 20K06857Japan Society for the Promotion of Science JSPS KAKENHI 22K15660
6 · The paper itself

Abstract

Neurotrophins are a family of secreted proteins expressed in the peripheral nervous system and the central nervous system that support neuronal survival, synaptic plasticity, and neurogenesis. Brain-derived neurotrophic factor (BDNF) and its high affinity receptor TrkB are highly expressed in the cortical and hippocampal areas and play an essential role in learning and memory. The decline of cognitive function with aging is a major risk factor for cognitive diseases such as Alzheimer's disease. Therefore, an alteration of BDNF/TrkB signaling with aging and/or pathological conditions has been indicated as a potential mechanism of cognitive decline. In this review, we summarize the cellular function of neurotrophin signaling and review the current evidence indicating a pathological role of neurotrophin signaling, especially of BDNF/TrkB signaling, in the cognitive decline in aging and age-related cognitive diseases. We also review the therapeutic approach for cognitive decline by the upregulation of the endogenous BDNF/TrkB-system.

Indexed as

Brain-Derived Neurotrophic FactorCognitive DysfunctionCognitionHippocampusHumansNeurotrophin 3Receptor, trkBSignal TransductionBrain-Derived Neurotrophic FactorNeurotrophin 3Receptor, trkBagingAlzheimer’s diseasebrain-derived neurotrophic factorexerciseintracellular signaling

Identifiers

PMID35887075
PMCPMC9320180
OpenAlexW4285495860

What OpenQuestion 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 OpenQuestion graph.