Evidence map›Paper›PMID 37127251›Full record

ReviewBiochemical pharmacology2023

A perspective on autophagy and transcription factor EB in Alcohol-Associated Alzheimer's disease.

Chen Zhang, Hao Chen, Yssa Rodriguez, Xiaowen Ma, Russell H Swerdlow, Jianhua Zhang, Wen-Xing Ding

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
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

7 authors at 2 institutions in 1 country.

Chen ZhangDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Hao ChenDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Yssa RodriguezDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Xiaowen MaDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Russell H SwerdlowDepartment of Neurology, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Jianhua ZhangDepartment of Pathology, Division of Molecular Cellular Pathology, University of Alabama at Birmingham, 901 19th street South, Birmingham, AL 35294, USA.
Wen-Xing DingDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA; Department of Internal Medicine, Division of Gastroenterology, Hepatology & Motility, The University of Kansas Medical Center, Kansas City, KS 66160, USA. Electronic address: wxding@kumc.edu.
University of Kansas Medical Center · USUniversity of Alabama at Birmingham · US

Funding

University of Kansas Alzheimer's Disease Research Center (KU ADRC)P30AG072973 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Jaime Perales Puchalt · 2021 to 2026
$25.3M
Mechanisms regulating autophagy in alcohol-induced liver injuryR37AA020518 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Wen-Xing Ding · 2019 to 2026
$3.2M
Mechanisms of Impaired Lysosomal Biogenesis and Autophagy in Alcohol-Associated Alzheimer's DiseaseR01AG072895 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI DING, WEN-XING · 2020 to 2024
$1.9M
NIAAA NIH HHS R37 AA020518NIA NIH HHS P30 AG072973NIA NIH HHS R01 AG072895
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of progressive dementia and there is no truly efficacious treatment. Accumulating evidence indicates that impaired autophagic function for removal of damaged mitochondria and protein aggregates such as amyloid and tau protein aggregates may contribute to the pathogenesis of AD. Epidemiologic studies have implicated alcohol abuse in promoting AD, yet the underlying mechanisms are poorly understood. In this review, we discuss mechanisms of selective autophagy for mitochondria and protein aggregates and how these mechanisms are impaired by aging and alcohol consumption. We also discuss potential genetic and pharmacological approaches for targeting autophagy/mitophagy, as well as lysosomal and mitochondrial biogenesis, for the potential prevention and treatment of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAutophagyEthanolHumansMitophagyProtein AggregatesTranscription FactorsAmyloid beta-PeptidesEthanolProtein AggregatesTranscription FactorsAggrephagyMitochondriaMitophagyNADTFEB

Identifiers

PMID37127251
PMCPMC11009931
OpenAlexW4367396357

What OpenQuestion holds

Textmetadata
LicenceTDM
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.