Evidence map›Paper›PMID 34680141›Full record

ReviewBiomolecules2021

Mitochondrial Dysfunction, Protein Misfolding and Neuroinflammation in Parkinson's Disease: Roads to Biomarker Discovery.

Anna Picca, Flora Guerra, Riccardo Calvani, Roberta Romano, Hélio José Coelho-Júnior, Cecilia Bucci, Emanuele Marzetti

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 3 pooled it
9.0field-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

92 citing papers in PubMed, 3 syntheses or guidelines pooled it, 148 citations in OpenAlex.

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32 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

7 authors at 3 institutions in 2 countries.

Anna PiccaFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.ORCID 0000-0001-7032-3487
Flora GuerraDepartment of Biological and Environmental Sciences and Technologies, Università del Salento, 73100 Lecce, Italy.ORCID 0000-0003-3379-7469
Riccardo CalvaniFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.
Roberta RomanoDepartment of Biological and Environmental Sciences and Technologies, Università del Salento, 73100 Lecce, Italy.ORCID 0000-0002-4987-3561
Hélio José Coelho-JúniorDepartment of Geriatrics and Orthopedics, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.ORCID 0000-0001-7482-9514
Cecilia BucciDepartment of Biological and Environmental Sciences and Technologies, Università del Salento, 73100 Lecce, Italy.ORCID 0000-0002-6232-6183
Emanuele MarzettiFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.ORCID 0000-0001-9567-6983
University of Salento · ITStockholm University · SEUniversità Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's Disease (PD) is a highly prevalent neurodegenerative disease among older adults. PD neuropathology is marked by the progressive loss of the dopaminergic neurons of the substantia nigra pars compacta and the widespread accumulation of misfolded intracellular α-synuclein (α-syn). Genetic mutations and post-translational modifications, such as α-syn phosphorylation, have been identified among the multiple factors supporting α-syn accrual during PD. A decline in the clearance capacity of the ubiquitin-proteasome and the autophagy-lysosomal systems, together with mitochondrial dysfunction, have been indicated as major pathophysiological mechanisms of PD neurodegeneration. The accrual of misfolded α-syn aggregates into soluble oligomers, and the generation of insoluble fibrils composing the core of intraneuronal Lewy bodies and Lewy neurites observed during PD neurodegeneration, are ignited by the overproduction of reactive oxygen species (ROS). The ROS activate the α-syn aggregation cascade and, together with the Lewy bodies, promote neurodegeneration. However, the molecular pathways underlying the dynamic evolution of PD remain undeciphered. These gaps in knowledge, together with the clinical heterogeneity of PD, have hampered the identification of the biomarkers that may be used to assist in diagnosis, treatment monitoring, and prognostication. Herein, we illustrate the main pathways involved in PD pathogenesis and discuss their possible exploitation for biomarker discovery.

Indexed as

alpha-SynucleinBiomarkersDopaminergic NeuronsHumansLewy BodiesMitochondriaNeuroinflammatory DiseasesParkinson DiseaseProtein AggregatesProteostasis DeficienciesReactive Oxygen Speciesalpha-SynucleinBiomarkersProtein AggregatesReactive Oxygen SpeciesSNCA protein, humanalpha-synucleinbeta-amyloid (Aβ)cytokineDAMPsextracellular vesiclesinflammationmitochondrial-derived vesiclesmitophagyneurofilaments light chain (NfL)p-tau pathology

Identifiers

PMID34680141
PMCPMC8534011
OpenAlexW3207118398

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.