Evidence map›Paper›PMID 33014536›Full record

ReviewAging and disease2020

A Glimmer of Hope: Maintain Mitochondrial Homeostasis to Mitigate Alzheimer's Disease.

Wenbo Li, Ling Kui, Tsirukis Demetrios, Xun Gong, Min Tang

Open access · goldAbstract readReview
In one paragraph

Review in Aging and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 19 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

5 authors at 5 institutions in 2 countries.

Wenbo Li1State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, China.
Ling Kui2Dana-Farber Cancer Institute, Harvard Medical School, United States.
Tsirukis Demetrios3Boston Children's Hospital, Harvard Medical School, United States.
Xun Gong4Department of Rheumatology & Immunology, The First Affiliated Hospital of Anhui Medical University, China.
Min Tang5Institute of Life Sciences, Jiangsu University, China.
Boston Children's Hospital · USCenter for Innovation · USFirst Affiliated Hospital of Anhui Medical University · CNHarvard University · USPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are classically known to be cellular energy producers. Given the high-energy demanding nature of neurons in the brain, it is essential that the mitochondrial pool remains healthy and provides a continuous and efficient supply of energy. However, mitochondrial dysfunction is inevitable in aging and neurodegenerative diseases. In Alzheimer's disease (AD), neurons experience unbalanced homeostasis like damaged mitochondrial biogenesis and defective mitophagy, with the latter promoting the disease-defining amyloid β (Aβ) and p-Tau pathologies impaired mitophagy contributes to inflammation and the aggregation of Aβ and p-Tau-containing neurotoxic proteins. Interventions that restore defective mitophagy may, therefore, alleviate AD symptoms, pointing out the possibility of a novel therapy. This review aims to illustrate mitochondrial biology with a focus on mitophagy and propose strategies to treat AD while maintaining mitochondrial homeostasis.

Indexed as

Alzheimer’s diseasemitochondria dysfunctionmitophagyNAD+

Identifiers

PMID33014536
PMCPMC7505280
OpenAlexW3088409236

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.