Evidence map›Paper›PMID 33327665›Full record

ReviewInternational journal of molecular sciences2020

Molecular Dysfunctions of Mitochondria-Associated Membranes (MAMs) in Alzheimer's Disease.

Fanny Eysert, Paula Fernanda Kinoshita, Arnaud Mary, Loan Vaillant-Beuchot, Frédéric Checler, Mounia Chami

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. NMolecular neurobiology · 2026
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  14. CoQAntioxidants (Basel, Switzerland) · 2024
    Review
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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

6 authors at 1 institution in 2 countries.

Fanny EysertUniversité Côte d'Azur, INSERM, CNRS, Institut of Molecular and Cellular Pharmacology, Laboratory of Excellence DistalZ, Sophia-Antipolis, 06560 Valbonne, France.
Paula Fernanda KinoshitaUniversité Côte d'Azur, INSERM, CNRS, Institut of Molecular and Cellular Pharmacology, Laboratory of Excellence DistalZ, Sophia-Antipolis, 06560 Valbonne, France.
Arnaud MaryUniversité Côte d'Azur, INSERM, CNRS, Institut of Molecular and Cellular Pharmacology, Laboratory of Excellence DistalZ, Sophia-Antipolis, 06560 Valbonne, France.
Loan Vaillant-BeuchotUniversité Côte d'Azur, INSERM, CNRS, Institut of Molecular and Cellular Pharmacology, Laboratory of Excellence DistalZ, Sophia-Antipolis, 06560 Valbonne, France.
Frédéric CheclerUniversité Côte d'Azur, INSERM, CNRS, Institut of Molecular and Cellular Pharmacology, Laboratory of Excellence DistalZ, Sophia-Antipolis, 06560 Valbonne, France.
Mounia ChamiUniversité Côte d'Azur, INSERM, CNRS, Institut of Molecular and Cellular Pharmacology, Laboratory of Excellence DistalZ, Sophia-Antipolis, 06560 Valbonne, France.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a multifactorial neurodegenerative pathology characterized by a progressive decline of cognitive functions. Alteration of various signaling cascades affecting distinct subcellular compartment functions and their communication likely contribute to AD progression. Among others, the alteration of the physical association between the endoplasmic reticulum (ER) and mitochondria, also reffered as mitochondria-associated membranes (MAMs), impacts various cellular housekeeping functions such as phospholipids-, glucose-, cholesterol-, and fatty-acid-metabolism, as well as calcium signaling, which are all altered in AD. Our review describes the physical and functional proteome crosstalk between the ER and mitochondria and highlights the contribution of distinct molecular components of MAMs to mitochondrial and ER dysfunctions in AD progression. We also discuss potential strategies targeting MAMs to improve mitochondria and ER functions in AD.

Indexed as

Alzheimer DiseaseAnimalsEndoplasmic ReticulumEndoplasmic Reticulum StressHumansMitochondriaMitochondrial MembranesAlzheimer’s disease (AD)Amyloid β peptide (Aβ)APOEAPP-C-terminal fragments (APP-CTFs)calcium signalingcholesterolEndoplasmic Reticulum (ER)fatty acidlipidsmitochondriaMitochondria-Associated Membranes (MAMs)phospholipidstauunfolded protein responseUnfolded Protein Response (UPR)β amyloid precursor protein (APP)

Identifiers

PMID33327665
PMCPMC7765134
OpenAlexW3112218303

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.