Evidence map›Paper›PMID 37298443›Full record

ReviewInternational journal of molecular sciences2023

Alcohol as a Modifiable Risk Factor for Alzheimer's Disease-Evidence from Experimental Studies.

Devaraj V Chandrashekar, Ross A Steinberg, Derick Han, Rachita K Sumbria

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 40 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Devaraj V ChandrashekarDepartment of Biomedical and Pharmaceutical Sciences, School of Pharmacy, Chapman University, Irvine, CA 92618, USA.
Ross A SteinbergSchool of Pharmacy and Health Sciences, Keck Graduate Institute, Claremont, CA 91711, USA.ORCID 0000-0002-3530-2557
Derick HanSchool of Pharmacy and Health Sciences, Keck Graduate Institute, Claremont, CA 91711, USA.
Rachita K SumbriaDepartment of Biomedical and Pharmaceutical Sciences, School of Pharmacy, Chapman University, Irvine, CA 92618, USA.ORCID 0000-0002-7459-0723
Chapman University · USKeck Graduate Institute · US

Funding

Modulation of the liver-brain axis by alcohol and its impact on Alzheimers disease pathologyR01AG072896 · NIA · KECK GRADUATE INST OF APPLIED LIFE SCIS · PI HAN, DERICK S, SUMBRIA, RACHITA · 2020 to 2024
$2.3M
A Brain Penetrating Bi-functional Transferrin Receptor Antibody-TNF-alpha Decoy Receptor Fusion Protein for Alzheimer's DiseaseR01AG062840 · NIA · KECK GRADUATE INST OF APPLIED LIFE SCIS · PI SUMBRIA, RACHITA · 2019 to 2024
$1.9M
NIA NIH HHS R01 AG062840NIA NIH HHS R01AG062840NIA NIH HHS R01 AG072896NIA NIH HHS R01AG072896
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by cognitive impairment and memory loss. Epidemiological evidence suggests that heavy alcohol consumption aggravates AD pathology, whereas low alcohol intake may be protective. However, these observations have been inconsistent, and because of methodological discrepancies, the findings remain controversial. Alcohol-feeding studies in AD mice support the notion that high alcohol intake promotes AD, while also hinting that low alcohol doses may be protective against AD. Chronic alcohol feeding to AD mice that delivers alcohol doses sufficient to cause liver injury largely promotes and accelerates AD pathology. The mechanisms by which alcohol can modulate cerebral AD pathology include Toll-like receptors, protein kinase-B (Akt)/mammalian target of rapamycin (mTOR) pathway, cyclic adenosine monophosphate (cAMP) response element-binding protein phosphorylation pathway, glycogen synthase kinase 3-β, cyclin-dependent kinase-5, insulin-like growth factor type-1 receptor, modulation of β-amyloid (Aβ) synthesis and clearance, microglial mediated, and brain endothelial alterations. Besides these brain-centric pathways, alcohol-mediated liver injury may significantly affect brain Aβ levels through alterations in the peripheral-to-central Aβ homeostasis. This article reviews published experimental studies (cell culture and AD rodent models) to summarize the scientific evidence and probable mechanisms (both cerebral and hepatic) by which alcohol promotes or protects against AD progression.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalEthanolMammalsMiceMice, TransgenicRisk FactorsAmyloid beta-PeptidesEthanolalcoholAlzheimer’s diseaseanimal modelscell cultureliver injuryliver steatosisβ-amyloid

Identifiers

PMID37298443
PMCPMC10253673
OpenAlexW4378906144

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.