Evidence map›Paper›PMID 33805142›Full record

ReviewInternational journal of molecular sciences2021

Alzheimer's Disease Pathogenesis: Role of Autophagy and Mitophagy Focusing in Microglia.

Mehdi Eshraghi, Aida Adlimoghaddam, Amir Mahmoodzadeh, Farzaneh Sharifzad, Hamed Yasavoli-Sharahi, Shahrokh Lorzadeh, Benedict C Albensi, Saeid Ghavami

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 2 pooled it
10.5field-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

87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 143 citations in OpenAlex.

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27 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

8 authors at 6 institutions in 4 countries.

Mehdi EshraghiCenter for Motor Neuron Biology and Disease, Columbia University, New York, NY 10032, USA.ORCID 0000-0002-5321-3849
Aida AdlimoghaddamSt. Boniface Hospital Albrechtsen Research Centre, Division of Neurodegenerative Disorders, Winnipeg, MB R2H2A6, Canada.
Amir MahmoodzadehMedical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah 6734667149, Iran.ORCID 0000-0002-0523-8152
Farzaneh SharifzadDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.ORCID 0000-0002-7959-4440
Hamed Yasavoli-SharahiDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.ORCID 0000-0002-2491-0709
Shahrokh LorzadehDepartment of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, Canada.
Benedict C AlbensiSt. Boniface Hospital Albrechtsen Research Centre, Division of Neurodegenerative Disorders, Winnipeg, MB R2H2A6, Canada.
Saeid GhavamiDepartment of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, Canada.ORCID 0000-0001-5948-508X
St. Boniface Hospital · CAUniversity of Ottawa · CACancerCare Manitoba · CAColumbia University · USKermanshah University of Medical Sciences · IRUniversity of Manitoba · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a debilitating neurological disorder, and currently, there is no cure for it. Several pathologic alterations have been described in the brain of AD patients, but the ultimate causative mechanisms of AD are still elusive. The classic hallmarks of AD, including amyloid plaques (Aβ) and tau tangles (tau), are the most studied features of AD. Unfortunately, all the efforts targeting these pathologies have failed to show the desired efficacy in AD patients so far. Neuroinflammation and impaired autophagy are two other main known pathologies in AD. It has been reported that these pathologies exist in AD brain long before the emergence of any clinical manifestation of AD. Microglia are the main inflammatory cells in the brain and are considered by many researchers as the next hope for finding a viable therapeutic target in AD. Interestingly, it appears that the autophagy and mitophagy are also changed in these cells in AD. Inside the cells, autophagy and inflammation interact in a bidirectional manner. In the current review, we briefly discussed an overview on autophagy and mitophagy in AD and then provided a comprehensive discussion on the role of these pathways in microglia and their involvement in AD pathogenesis.

Indexed as

AutophagyMitophagyAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainComplement System ProteinsHumansInflammationMiceMice, TransgenicMicrogliaMitochondriaNeurodegenerative DiseasesNeuronsReceptors, FcAmyloid beta-PeptidesComplement System ProteinsReceptors, FcReceptors, Scavengertau ProteinsAlzheimer’sautophagyinflammationmicrogliamitochondriamitophagyneurodegenerationneuroinflammation

Identifiers

PMID33805142
PMCPMC8036323
OpenAlexW3139044132

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.