Evidence map›Paper›PMID 34472487›Full record

ArticleNeural regeneration research2022

Striatal oxidative damages and neuroinflammation correlate with progression and survival of Lewy body and Alzheimer diseases.

Huifangjie Li, William C Knight, Jinbin Xu

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 15 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

3 authors at 1 institution in 1 country.

Huifangjie LiDepartment of Radiology, Washington University School of Medicine, St. Louis, MO, USA.
William C KnightDepartment of Radiology, Washington University School of Medicine, St. Louis, MO, USA.
Jinbin XuDepartment of Radiology, Washington University School of Medicine, St. Louis, MO, USA.
Washington University in St. Louis · US

Funding

Dissect the mechanisms of selective regional vulnerability in Lewy Body Dementias via comparative snRNA-seq analysisR01NS123571 · NINDS · WASHINGTON UNIVERSITY · PI XU, JINBIN, ZHAO, GUOYAN · 2021 to 2025
$3.6M
POSTMORTEM VALIDATION OF BIOMARKERS FOR IMAGING PARKINSON DISEASER01NS092865 · NINDS · WASHINGTON UNIVERSITY · PI XU, JINBIN · 2016 to 2020
$1.7M
Define molecular events driving selective neuronal death in multiple neurodegenerative diseases by snRNA-seqR03AG070474 · NIA · WASHINGTON UNIVERSITY · PI XU, JINBIN, ZHAO, GUOYAN · 2021 to 2022
$315k
DOPAMINE D1, D2, AND D3 RECEPTORS AS BIOMARKERS FOR IMAGING NIGROSTRIATAL NEURONSR03NS090214 · NINDS · WASHINGTON UNIVERSITY · PI XU, JINBIN · 2014 to 2015
$153k
NIA NIH HHS R03 AG070474NINDS NIH HHS R01 NS092865NINDS NIH HHS R01 NS123571NINDS NIH HHS R03 NS090214
6 · The paper itself

Abstract

Neurodegenerative diseases are a class of chronic and complex disorders featuring progressive loss of neurons in distinct brain areas. The mechanisms responsible for the disease progression in neurodegeneration are not fully illustrated. In this observational study, we have examined diverse biochemical parameters in the caudate and putamen of patients with Lewy body diseases (LBDs) and Alzheimer disease (AD), shedding some light on the involvement of oxidative damage and neuroinflammation in advanced neurodegeneration. We performed Spearman and Mantel-Cox analyses to investigate how oxidative stress and neuroinflammation exert comprehensive effects on disease progression and survival. Disease progression in LBDs correlated positively with poly (ADP-Ribose) and triggering receptors expressed on myeloid cell 2 levels in the striatum of LBD cohorts, indicating that potential parthanatos was a dominant feature of worsening disease progression and might contribute to switching microglial inflammatory phenotypes. Disease progression in AD corresponds negatively with 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG) and myeloperoxidase concentrations in the striatum, suggesting that possible mitochondria dysfunction may be involved in the progression of AD via a mechanism of β-amyloid entering the mitochondria and subsequent free radicals generation. Patients with lower striatal 8-oxo-dG and myeloperoxidase levels had a survival advantage in AD. The age of onset also affected disease progression. Tissue requests for the postmortem biochemistry, genetics, and autoradiography studies were approved by the Washington University Alzheimer's Disease Research Center (ADRC) Biospecimens Committee (ethics approval reference number: T1705, approval date: August 6, 2019). Recombinant DNA and Hazardous Research Materials were approved by the Washington University Environmental Health & Safety Biological Safety Committee (approval code: 3739, approval date: February 25, 2020). Radioactive Material Authorization was approved by the Washington University Environmental Health & Safety Radiation Safety Committee (approval code: 1056, approval date: September 18, 2019).

Indexed as

Alzheimer diseasedisease progressionLewy body diseasesmicroglianeurodegenerationoxidative damagestriatumsurvival

Identifiers

PMID34472487
PMCPMC8530139
OpenAlexW3196793010

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.