Evidence map›Paper›PMID 26343025›Full record

ArticleAging2015

Metabolic profiling distinguishes three subtypes of Alzheimer's disease.

Dale E Bredesen

Open access · hybridAbstract readCase Reports
In one paragraph

Article in Aging, 2015. 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
4.7field-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

42 citing papers in PubMed, 81 citations in OpenAlex.

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  12. How Can Insulin Resistance Cause Alzheimer's Disease?International journal of molecular sciences · 2023
    Review
  13. Association between dietary zinc intake andFrontiers in nutrition · 2023
    Article
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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

1 author at 1 institution in 1 country.

Dale E BredesenMary S. Easton Center for Alzheimer's Disease Research, Department of Neurology, University of California, Los Angeles, CA 90095, USA.
Foundation for Psychocultural Research · US

Funding

UCLA ALZHEIMERS DISEASE RESEARCH CENTERP50AG016570 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CUMMINGS, JEFFREY L. · 1999 to 2014
$25.9M
Novel Prionic Mechanism Underlying Alzheimer?s DiseaseR01AG034427 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI BREDESEN, DALE E. · 2009 to 2012
$1.5M
APP signaling networkR21AG036975 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI BREDESEN, DALE E. · 2012 to 2013
$520k
NIA NIH HHS AG034427NIA NIH HHS AG036975NIA NIH HHS AG16570NIA NIH HHS P50 AG016570NIA NIH HHS R01 AG034427NIA NIH HHS R21 AG036975
6 · The paper itself

Abstract

The cause of Alzheimer's disease is incompletely defined, and no truly effective therapy exists. However, multiple studies have implicated metabolic abnormalities such as insulin resistance, hormonal deficiencies, and hyperhomocysteinemia. Optimizing metabolic parameters in a comprehensive way has yielded cognitive improvement, both in symptomatic and asymptomatic individuals. Therefore, expanding the standard laboratory evaluation in patients with dementia may be revealing. Here I report that metabolic profiling reveals three Alzheimer's disease subtypes. The first is inflammatory, in which markers such as hs-CRP and globulin:albumin ratio are increased. The second type is non-inflammatory, in which these markers are not increased, but other metabolic abnormalities are present. The third type is a very distinctive clinical entity that affects relatively young individuals, extends beyond the typical Alzheimer's disease initial distribution to affect the cortex widely, is characterized by early non-amnestic features such as dyscalculia and aphasia, is often misdiagnosed or labeled atypical Alzheimer's disease, typically affects ApoE4-negative individuals, and is associated with striking zinc deficiency. Given the involvement of zinc in multiple Alzheimer's-related metabolic processes, such as insulin resistance, chronic inflammation, ADAM10 proteolytic activity, and hormonal signaling, this syndrome of Alzheimer's-plus with low zinc (APLZ) warrants further metabolic, genetic, and epigenetic characterization.

Indexed as

AgedAlzheimer DiseaseFemaleHumansMaleMetabolomeMiddle AgedZincZincbiomarkerscognitiondementiadyscalculiainflammationinsulin resistanceneurodegeneration

Identifiers

PMID26343025
PMCPMC4586104
OpenAlexW1798009377

What OpenQuestion holds

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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.