Evidence map›Paper›PMID 30776001›Full record

ReviewJournal of Alzheimer's disease : JAD2019

Therapeutic Potential of AMP-Activated Protein Kinase in Alzheimer's Disease.

Xin Wang, Helena R Zimmermann, Tao Ma

Abstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
–field-weighted citation impact
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

42 citing papers in PubMed.

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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

3 authors.

Xin WangDepartment of Internal Medicine, Gerontology & Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Helena R ZimmermannDepartment of Internal Medicine, Gerontology & Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Tao MaDepartment of Internal Medicine, Gerontology & Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.

Funding

Wake Forest Alzheimer's Disease Core CenterP30AG049638 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CRAFT, SUZANNE · 2016 to 2020
$12.2M
Isoform-specific roles of AMPK in synaptic failure and memory deficit in Alzheimer's DiseaseR01AG055581 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2017 to 2021
$2.9M
Role of protein synthesis in Alzheimers disease-associated impairments of synaptic plasticity and memoryR01AG056622 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2017 to 2021
$2.4M
AMPK in Alzheimer's Disease-Associated Synaptic Failure and Memory DeficitsR00AG044469 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2015 to 2017
$739k
AMPK in Alzheimer's Disease-Associated Synaptic Failure and Memory DeficitsK99AG044469 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2013 to 2014
$171k
Elucidating the roles of AMPK isoforms in Alzheimer's Disease PathogenesisF31AG055264 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ZIMMERMANN, HELENA ROSE · 2017 to 2018
$80k
NIA NIH HHS F31 AG055264NIA NIH HHS K99 AG044469NIA NIH HHS P30 AG049638NIA NIH HHS R00 AG044469NIA NIH HHS R01 AG055581NIA NIH HHS R01 AG056622
6 · The paper itself

Abstract

Currently there is no cure or effective disease-modifying therapy for Alzheimer's disease (AD), the most common form of dementia that is becoming a global threat to public health. It is important to develop novel therapeutic strategies targeting AD pathophysiology particularly synaptic failure and cognitive impairments. Recent studies revealed several molecular signaling pathways potentially linked to brain pathology and synaptic failure in AD, including AMP-activated protein kinase (AMPK), a master kinase that plays a central role in the maintenance of cellular energy homeostasis. Particularly, hyperactive AMPK via phosphorylation has been linked to AD-associated synaptic plasticity impairments, indicating suppression of AMPK activity might be beneficial for cognitive deficiency in AD. In this review, we will discuss how targeting dysregulation of AMPK signaling could be a feasible therapeutic approach for AD.

Indexed as

Alzheimer DiseaseAMP-Activated Protein KinasesAnimalsBrainHumansNeuronal PlasticityProtein Kinase InhibitorsSignal Transductiontau ProteinsAMP-Activated Protein KinasesProtein Kinase Inhibitorstau ProteinsAlzheimer’s diseaseAMPKprotein synthesissignaling transductionsynaptic plasticity

Identifiers

PMID30776001
PMCPMC6446925

What OpenQuestion holds

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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.