Evidence map›Paper›PMID 39766244›Full record

ArticleBiomolecules2024

Late-Life Alcohol Exposure Does Not Exacerbate Age-Dependent Reductions in Mouse Spatial Memory and Brain TFEB Activity.

Hao Chen, Kaitlyn Hinz, Chen Zhang, Yssa Rodriguez, Sha Neisha Williams, Mengwei Niu, Xiaowen Ma, Xiaojuan Chao, Alexandria L Frazier, Kenneth E McCarson and 7 more

Abstract read
In one paragraph

Article in Biomolecules, 2024. 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
–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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Hao ChenDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.ORCID 0000-0002-9179-5720
Kaitlyn HinzDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.ORCID 0000-0003-1081-3518
Chen ZhangDepartment 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.
Sha Neisha WilliamsDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Mengwei NiuDepartment 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.
Xiaojuan ChaoDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Alexandria L FrazierR.L. Smith IDDRC Rodent Behavior Facility, Disease Model and Assessment Services, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Kenneth E McCarsonDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.ORCID 0000-0002-0175-7297
Xiaowan WangDepartment of Neurology, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Zheyun PengDepartment of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Detroit, MI 48201, USA.
Wanqing LiuDepartment of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Detroit, MI 48201, USA.ORCID 0000-0001-7727-6900
Hong-Min NiDepartment of Pharmacology, Toxicology and Therapeutics, 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.ORCID 0000-0002-2128-9574
Russell H SwerdlowDepartment of Neurology, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Wen-Xing DingDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.

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
Using PCORnet to Expand the DS-CONNECT Cohort Through Healthcare System Recruitment, Incorporating Electronic Health Records, and Assessing Self-DeterminationU54HD090216 · NICHD · UNIVERSITY OF KANSAS LAWRENCE · PI COLOMBO, JOHN A. · 2016 to 2020
$6.2M
Mechanisms regulating autophagy in alcohol-induced liver injuryR37AA020518 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Wen-Xing Ding · 2019 to 2026
$3.2M
A Precision Medicine for Alcohol-Associated Liver DiseaseUT2AA031151 · NIAAA · GENETOBE INC. · PI BISGAIER, CHARLES LARRY, LIU, WANQING · 2023 to 2024
$2.0M
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
A Precision Targeted Therapeutics for Nonalcoholic Fatty Liver DiseaseR01DK124612 · NIDDK · WAYNE STATE UNIVERSITY · PI LIU, WANQING · 2021 to 2024
$1.7M
NIAAA NIH HHS R37 AA020518NIAAA NIH HHS UT2 AA031151NIA NIH HHS P30 AG072973NIA NIH HHS R01 AG072895NICHD NIH HHS U54 HD090216NIDDK NIH HHS R01 DK124612NIH HHS NICHD HD090216Wanqing Liu 1UT2AA031151Wanqing Liu R01DK124612
6 · The paper itself

Abstract

Alcohol consumption is believed to affect Alzheimer's disease (AD) risk, but the contributing mechanisms are not well understood. A potential mediator of the proposed alcohol-AD connection is autophagy, a degradation pathway that maintains organelle and protein homeostasis. Autophagy is regulated through the activity of Transcription factor EB (TFEB), which promotes lysosome and autophagy-related gene expression. The purpose of this study is to explore whether chronic alcohol consumption worsens the age-related decline in TFEB-mediated lysosomal biogenesis in the brain and exacerbates cognitive decline associated with aging. To explore the effect of alcohol on brain TFEB and autophagy, we exposed young (3-month-old) and aged (23-month-old) mice to two alcohol-feeding paradigms and assessed biochemical, transcriptome, histology, and behavioral endpoints. In young mice, alcohol decreased hippocampal nuclear TFEB staining but increased SQSTM1/p62, LC3-II, ubiquitinated proteins, and phosphorylated Tau. Hippocampal TFEB activity was lower in aged mice than it was in young mice, and Gao-binge alcohol feeding did not worsen the age-related reduction in TFEB activity. Morris Water and Barnes Maze spatial memory tasks were used to characterize the effects of aging and chronic alcohol exposure (mice fed alcohol for 4 weeks). The aged mice showed worse spatial memory acquisition in both tests. Alcohol feeding slightly impaired spatial memory in the young mice, but had little effect or even slightly improved spatial memory acquisition in the aged mice. In conclusion, aging produces greater reductions in brain autophagy flux and impairment of spatial memory than alcohol consumption.

Indexed as

AgingBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBrainEthanolSpatial MemoryAlcohol DrinkingAnimalsAutophagyHippocampusMaleMiceMice, Inbred C57BLBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsEthanolTcfeb protein, mouseautophagylipidlysosomemitochondriatau aggregation

Identifiers

PMID39766244
PMCPMC11673978

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.