Evidence map›Paper›PMID 32444538›Full record

ArticleJournal of Alzheimer's disease : JAD2020

Decreased Levels of Blood AMPKα1 but not AMPKα2 Isoform in Patients with Mild Cognitive Impairment and Alzheimer's Disease: A Pilot Study.

Xin Wang, Helena R Zimmermann, Samuel N Lockhart, Suzanne Craft, Tao Ma

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  6. Aberrant Energy Metabolism in Alzheimer's Disease.Journal of translational internal medicine · 2022
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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 1 institution in 1 country.

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.
Samuel N LockhartDepartment of Internal Medicine, Gerontology & Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Suzanne CraftDepartment 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.
Wake Forest University · US

Funding

Wake Forest Alzheimer's Disease Core CenterP30AG049638 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RAPP, STEPHEN R · 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
NIA NIH HHS P30 AG049638NIA NIH HHS R01 AG055581NIA NIH HHS R01 AG056622
6 · The paper itself

Abstract

backgroundThere is an urgent need to develop feasible biomarkers for diagnosis and prognosis of Alzheimer's disease (AD). Mounting evidence implicates that dysregulation of energy metabolism is a key and early event in AD pathogenesis. AMP-activated protein kinase (AMPK) is a central molecular sensor that plays a critical role in maintaining cellular energy homeostasis, and aberrant brain AMPK activities are linked to AD pathophysiology.

objectiveWe aimed to investigated protein levels of AMPKα isoforms, AMPKα1 and AMPKα2, in plasma samples from patients clinically diagnosed with mild cognitive impairment (MCI) or AD, along with age-matched healthy controls.

methods30 participants (10 MCI, 10 AD, and 10 controls) were included in our pilot study. Plasma levels of AMPKα1 and AMPKα2 were determined by ELISA. Receiver operating characteristic (ROC) analysis was used to assess sensitivity and specificity. Linear regression was used to assess the correlation between levels of AMPKα isoforms and other biomarkers.

resultsPlasma levels of AMPKα1 were decreased in MCI and AD patients, while levels of AMPKα2 were unaltered as compared to controls. ROC analysis showed relatively high sensitivity and specificity for AMPKα1 to distinguish MCI and AD from controls. Linear regression analysis showed that plasma levels of AMPKα1 were correlated with a brain imaging biomarker (AD signature cortical thicknesses).

conclusionPlasma levels of AMPKα1 were decreased in MCI and AD patients. Future endeavor to explore whether blood AMPKα1 protein expression has the value as a potential biomarker for AD and MCI diagnosis shall be encouraged.

Indexed as

AgedAlzheimer DiseaseAMP-Activated Protein KinasesBiomarkersCognitive DysfunctionFemaleHumansIsoenzymesMagnetic Resonance ImagingMaleMiddle AgedNeuropsychological TestsPilot ProjectsAMP-Activated Protein KinasesBiomarkersIsoenzymesPRKAA1 protein, humanPRKAA2 protein, humanAlzheimer’s diseaseAMPKbiomarkerisoformmild cognitive impairmentplasma

Identifiers

PMID32444538
PMCPMC8009325
OpenAlexW3027441575

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.