Evidence map›Paper›PMID 32895786›Full record

ArticleMolecular neurobiology2021

DNA Double-Strand Break Accumulation in Alzheimer's Disease: Evidence from Experimental Models and Postmortem Human Brains.

Nidheesh Thadathil, David F Delotterie, Jianfeng Xiao, Roderick Hori, Michael P McDonald, Mohammad Moshahid Khan

Abstract read
In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

67 citing papers in PubMed, 86 citations in OpenAlex.

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7 more citing papers are in PubMed but not listed here.

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.

Nidheesh ThadathilDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, 415 Link Building, Memphis, TN, 38163, USA.
David F DelotterieDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, 415 Link Building, Memphis, TN, 38163, USA.
Jianfeng XiaoDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, 415 Link Building, Memphis, TN, 38163, USA.
Roderick HoriDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA.
Michael P McDonaldDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, 415 Link Building, Memphis, TN, 38163, USA.
Mohammad Moshahid KhanDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, 415 Link Building, Memphis, TN, 38163, USA. mkhan26@uthsc.edu.ORCID http://orcid.org/0000-0003-4679-294X
University of Tennessee Health Science Center · US

Funding

Effects of glycomacropeptide on memory and Alzheimer-related neuropathologyR01AG054562 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MCDONALD, MICHAEL P · 2017 to 2020
$1.5M
Effects of intracranial rAAV.Neu3 on dementia and neuropathologyR21AG051032 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LIAO, FRANCESCA-FANG, MCDONALD, MICHAEL P · 2016 to 2017
$418k
NIA NIH HHS R01 AG054562NIA NIH HHS R21 AG051032U.S. Department of Defense W81XWH-17-1-0062
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease that accounts for a majority of dementia cases. AD is characterized by progressive neuronal death associated with neuropathological lesions consisting of neurofibrillary tangles and senile plaques. While the pathogenesis of AD has been widely investigated, significant gaps in our knowledge remain about the cellular and molecular mechanisms promoting AD. Recent studies have highlighted the role of DNA damage, particularly DNA double-strand breaks (DSBs), in the progression of neuronal loss in a broad spectrum of neurodegenerative diseases. In the present study, we tested the hypothesis that accumulation of DNA DSB plays an important role in AD pathogenesis. To test our hypothesis, we examined DNA DSB expression and DNA repair function in the hippocampus of human AD and non-AD brains by immunohistochemistry, ELISA, and RT-qPCR. We observed increased DNA DSB accumulation and reduced DNA repair function in the hippocampus of AD brains compared to the non-AD control brains. Next, we found significantly increased levels of DNA DSB and altered levels of DNA repair proteins in the hippocampus of 5xFAD mice compared to non-transgenic mice. Interestingly, increased accumulation of DNA DSBs and altered DNA repair proteins were also observed in cellular models of AD. These findings provided compelling evidence that AD is associated with accumulation of DNA DSB and/or alteration in DSB repair proteins which may influence an important early part of the pathway toward neural damage and memory loss in AD.

Indexed as

DNA Breaks, Double-StrandedPostmortem ChangesAlzheimer DiseaseAnimalsBrainCells, CulturedCHO CellsCricetulusDisease Models, AnimalDNA RepairHippocampusHumansMice, TransgenicAlzheimer’s diseaseAmyloid betaDNA damageDNA repairNeurodegeneration

Identifiers

PMID32895786
PMCPMC13252816
OpenAlexW3084100386

What OpenQuestion holds

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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.