Evidence map›Paper›PMID 32445085›Full record

ReviewMolecular neurobiology2020

The Role of Mitochondria in Neurodegenerative Diseases: the Lesson from Alzheimer's Disease and Parkinson's Disease.

Giacomo Monzio Compagnoni, Alessio Di Fonzo, Stefania Corti, Giacomo P Comi, Nereo Bresolin, Eliezer Masliah

Open access · greenAbstract readReview
In one paragraph

Review in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
204citing papers in PubMed, 5 pooled it
15.8field-weighted citation impact, top 1% 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

204 citing papers in PubMed, 5 syntheses or guidelines pooled it, 367 citations in OpenAlex.

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  19. Heterotrimetallic Au@CuMaterials today. Bio · 2026
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144 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 4 institutions in 2 countries.

Giacomo Monzio CompagnoniIRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy. gmonziocompagnoni@bwh.harvard.edu.ORCID http://orcid.org/0000-0001-5323-8766
Alessio Di FonzoIRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Stefania CortiIRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Giacomo P ComiIRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Nereo BresolinIRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Eliezer MasliahDivision of Neuroscience and Laboratory of Neurogenetics, National Institute on Aging, National Institute of Health, Bethesda, MD, USA.
University of Milan · ITBrigham and Women's Hospital · USFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITNational Institute on Aging · US

Funding

Neuroimmune responses and therapeutics of alpha-synucleinopathies of the aging populationZIAAG000936 · NIA · NATIONAL INSTITUTE ON AGING · PI COOKSON, MARK · 2017 to 2025
$4.1M
Fresco Institute for Parkinson's and Movement Disorders not availableIntramural NIH HHS ZIA AG000936
6 · The paper itself

Abstract

Although the pathogenesis of neurodegenerative diseases is still widely unclear, various mechanisms have been proposed and several pieces of evidence are supportive for an important role of mitochondrial dysfunction. The present review provides a comprehensive and up-to-date overview about the role of mitochondria in the two most common neurodegenerative disorders: Alzheimer's disease (AD) and Parkinson's disease (PD). Mitochondrial involvement in AD is supported by clinical features like reduced glucose and oxygen brain metabolism and by numerous microscopic and molecular findings, including altered mitochondrial morphology, impaired respiratory chain function, and altered mitochondrial DNA. Furthermore, amyloid pathology and mitochondrial dysfunction seem to be bi-directionally correlated. Mitochondria have an even more remarkable role in PD. Several hints show that respiratory chain activity, in particular complex I, is impaired in the disease. Mitochondrial DNA alterations, involving deletions, point mutations, depletion, and altered maintenance, have been described. Mutations in genes directly implicated in mitochondrial functioning (like Parkin and PINK1) are responsible for rare genetic forms of the disease. A close connection between alpha-synuclein accumulation and mitochondrial dysfunction has been observed. Finally, mitochondria are involved also in atypical parkinsonisms, in particular multiple system atrophy. The available knowledge is still not sufficient to clearly state whether mitochondrial dysfunction plays a primary role in the very initial stages of these diseases or is secondary to other phenomena. However, the presented data strongly support the hypothesis that whatever the initial cause of neurodegeneration is, mitochondrial impairment has a critical role in maintaining and fostering the neurodegenerative process.

Indexed as

Alzheimer DiseaseAnimalsBrainDNA, MitochondrialElectron Transport Complex IHumansMitochondriaParkinson DiseaseDNA, MitochondrialElectron Transport Complex IAlzheimer’s diseaseMitochondriaNeurodegenerationParkinson’s diseasePathogenesis

Identifiers

PMID32445085
PMCPMC9047992
OpenAlexW3027900078

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.