Evidence map›Paper›PMID 26077923›Full record

ReviewNeurochemical research2015

Abnormal Glucose Metabolism in Alzheimer's Disease: Relation to Autophagy/Mitophagy and Therapeutic Approaches.

Kalpita Banerjee, Soumyabrata Munshi, David E Frank, Gary E Gibson

Open access · greenAbstract readReview
In one paragraph

Review in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  13. RapidChemical science · 2019
    Article
  14. Review
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  18. Resveratrol and Brain Mitochondria: a Review.Molecular neurobiology · 2018
    Review
  19. Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Kalpita BanerjeeBrain and Mind Research Institute, Weill Cornell Medical College, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY, 10605, USA.
Soumyabrata MunshiDepartment of Cellular and Molecular Pharmacology and Department of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL, 60064, USA.
David E FrankBrain and Mind Research Institute, Weill Cornell Medical College, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY, 10605, USA.
Gary E GibsonBrain and Mind Research Institute, Weill Cornell Medical College, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY, 10605, USA. ggibson@med.cornell.edu.
Burke Medical Research Institute · USRosalind Franklin University of Medicine and Science · US

Funding

TRANSCRIPTIONAL RESPONSES TO MITOCHONDRIAL DYSFUNCTIONP01AG014930 · NIA · WINIFRED MASTERSON BURKE MED RES INST · PI GIBSON, GARY E · 1999 to 2020
$30.7M
NIA NIH HHS AG14930NIA NIH HHS P01 AG014930
6 · The paper itself

Abstract

Diminished glucose metabolism accompanies many neurodegenerative diseases including Alzheimer's disease. An understanding of the relation of these metabolic changes to the disease will enable development of novel therapeutic strategies. Following a metabolic challenge, cells generally conserve energy to preserve viability. This requires activation of many cellular repair/regenerative processes such as mitophagy/autophagy and fusion/fission. These responses may diminish cell function in the long term. Prolonged fission induces mitophagy/autophagy which promotes repair but if prolonged progresses to mitochondrial degradation. Abnormal glucose metabolism alters protein signaling including the release of proteins from the mitochondria or migration of proteins from the cytosol to the mitochondria or nucleus. This overview provides an insight into the different mechanisms of autophagy/mitophagy and mitochondrial dynamics in response to the diminished metabolism that occurs with diseases, especially neurodegenerative diseases such as Alzheimer's disease. The review discusses multiple aspects of mitochondrial responses including different signaling proteins and pathways of mitophagy and mitochondrial biogenesis. Improving cellular bioenergetics and mitochondrial dynamics will alter protein signaling and improve cellular/mitochondrial repair and regeneration. An understanding of these changes will suggest new therapeutic strategies.

Indexed as

AutophagyMitophagyAlzheimer DiseaseAnimalsGlucoseHumansMitochondriaGlucoseFissionFusionGlucose metabolismMitophagy/autophagyNeurodegeneration

Identifiers

PMID26077923
PMCPMC4674363
OpenAlexW625404264

What OpenQuestion holds

Textmetadata
LicenceTDM
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.