Evidence mapPaperPMID 39583750Full record

ReviewInternational journal of physiology, pathophysiology and pharmacology2024

Caveolae with serotonin and NMDA receptors as promising targets for the treatment of Alzheimer's disease.

Moeka Nakashima, Naoko Suga, Akari Fukumoto, Sayuri Yoshikawa, Satoru Matsuda

Abstract readReview
In one paragraph

Review in International journal of physiology, pathophysiology and pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

5 authors.

Moeka NakashimaDepartment of Food Science and Nutrition, Nara Women's University Kita-Uoya Nishimachi, Nara 630-8506, Japan.
Naoko SugaDepartment of Food Science and Nutrition, Nara Women's University Kita-Uoya Nishimachi, Nara 630-8506, Japan.
Akari FukumotoDepartment of Food Science and Nutrition, Nara Women's University Kita-Uoya Nishimachi, Nara 630-8506, Japan.
Sayuri YoshikawaDepartment of Food Science and Nutrition, Nara Women's University Kita-Uoya Nishimachi, Nara 630-8506, Japan.
Satoru MatsudaDepartment of Food Science and Nutrition, Nara Women's University Kita-Uoya Nishimachi, Nara 630-8506, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is the most general type of cognitive impairments. Until recently, strategies that prevent its clinical progression have remained more elusive. Consequently, research direction should be for finding effective neuroprotective agents. It has been suggested oxidative stress, mitochondrial injury, and inflammation level might lead to brain cell death in many neurological disorders. Therefore, several autophagy-targeted bioactive compounds may be promising candidate therapeutics for the prevention of brain cell damage. Interestingly, some risk genes to Alzheimer's disease are expressed within brain cells, which may be linked to cholesterol metabolism, lipid transport, endocytosis, exocytosis and/or caveolae formation, suggesting that caveolae may be a fruitful therapeutic target to improve cognitive impairments. This review would highlight the latest advances in therapeutic technologies to improve the treatment of Alzheimer's disease. In particular, a paradigm that serotonin and N-methyl-d-aspartate (NMDA) receptors agonist/antagonist within caveolae structure might possibly improve the cognitive impairment. Consequently, cellular membrane biophysics should improve our understanding of the pathology of the cognitive dysfunction associated with Alzheimer's disease. Here, this research direction for the purpose of therapy may open the potential to move a clinical care toward disease-modifying treatment strategies with certain benefits for patients.

Indexed as

Alzheimer’s diseaseautophagyCaveolaecaveolincognitive impairmentglucagon-like peptide-1mitophagyNMDAserotonin

Identifiers

PMID39583750
PMCPMC11579522

What Socratic holds

Textmetadata
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.