Evidence map›Paper›PMID 35801276›Full record

ArticleAging cell2022

A partial reduction of VDAC1 enhances mitophagy, autophagy, synaptic activities in a transgenic Tau mouse model.

Murali Vijayan, Rainier Vladlen Alvir, Razelle Veronique Alvir, Lloyd E Bunquin, Jangampalli Adi Pradeepkiran, P Hemachandra Reddy

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 32 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

6 authors at 1 institution in 1 country.

Murali VijayanDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.ORCID 0000-0002-7426-3415
Rainier Vladlen AlvirDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.
Razelle Veronique AlvirDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.
Lloyd E BunquinDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.
Jangampalli Adi PradeepkiranDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.
P Hemachandra ReddyDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.ORCID 0000-0002-9560-9948
Texas Tech University · US

Funding

Mitochondrial Molecules in Alzheimer's Disease and Other TauopathiesR01AG069333 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2020 to 2023
$3.4M
Dynamin-Related Protein 1 and Mitochondrial Fragmentation in Alzheimer's DiseaseR01AG042178 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2012 to 2016
$2.0M
Voltage-Dependent Anion Channel and Neurodegeneration in Alzheimer's DiseaseR01AG047812 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2014 to 2018
$1.9M
Mitochondrial Fragmentation and Neurodegeneration in Huntington's DiseaseR01NS105473 · NINDS · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2017 to 2021
$1.8M
Small Molecules as Therapeutic Targets for Alzheimer's DiseaseR56AG060767 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2019 to 2019
$699k
MicroRNA-455-3p and Alzheimer's DiseaseR56AG066347 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2020 to 2020
$586k
Small Molecule Inhibitor Therapeutic Target for Alzheimer's Disease.R41AG060836 · NIA · SYNAPTEX, LLC · PI REDDY, P. HEMACHANDRA · 2018 to 2018
$250k
NIA NIH HHS R01 AG042178NIA NIH HHS R01 AG047812NIA NIH HHS R01 AG069333NIA NIH HHS R41 AG060836NIA NIH HHS R56 AG060767NIA NIH HHS R56 AG066347NINDS NIH HHS R01 NS105473
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of mental dementia in the aged population. AD is characterized by the progressive decline of memory and multiple cognitive functions, and changes in behavior and personality. Recent research has revealed age-dependent increased levels of VDAC1 in postmortem AD brains and cerebral cortices of APP, APPxPS1, and 3xAD.Tg mice. Further, we found abnormal interaction between VDAC1 and P-Tau in the AD brains, leading to mitochondrial structural and functional defects. Our current study aimed to understand the impact of a partial reduction of voltage-dependent anion channel 1 (VDAC1) protein on mitophagy/autophagy, mitochondrial and synaptic activities, and behavior changes in transgenic TAU mice in Alzheimer's disease. To determine if a partial reduction of VDAC1 reduces mitochondrial and synaptic toxicities in transgenic Tau (P301L) mice, we crossed heterozygote VDAC1 knockout (VDAC1

Indexed as

Alzheimer DiseaseAnimalsAutophagyDisease Models, AnimalMiceMice, TransgenicMitophagytau ProteinsVoltage-Dependent Anion Channel 1tau ProteinsVdac1 protein, mouseVoltage-Dependent Anion Channel 1Alzheimer's diseaseautophagyhexokinasesmitochondriamitochondrial biogenesismitophagyoxidative stressvoltage-dependent anion channel 1

Identifiers

PMID35801276
PMCPMC9381918
OpenAlexW4284971024

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.