Evidence map›Paper›PMID 20571935›Full record

ReviewNeuromolecular medicine2010

Alterations of the sphingolipid pathway in Alzheimer's disease: new biomarkers and treatment targets?

Michelle M Mielke, Constantine G Lyketsos

Open access · greenAbstract readReview
In one paragraph

Review in Neuromolecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
4.4field-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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Review
  6. Review
  7. Article
  8. Article
  9. Towards a Unitary Hypothesis of Alzheimer's Disease Pathogenesis.Journal of Alzheimer's disease : JAD · 2024
    Article
  10. Article
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  12. Review
  13. Article
  14. Article
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10 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Michelle M MielkeDivision of Geriatric Psychiatry and Neuropsychiatry, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Bayview, Alpha Commons Building, 4th floor, room 454, Baltimore, MD 21224, USA. mmielke1@jhmi.edu
Constantine G Lyketsos
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

'T V ASSESSMENT - MEMORY DISORDERED PATIENTS'P50AG005146 · NIA · JOHNS HOPKINS UNIVERSITY · PI TRONCOSO, JUAN · 1985 to 2019
$37.6M
Blood-based lipid biomarkers reflective of Alzheimer-associated neurodegenerationR21NS060271 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MIELKE, MICHELLE M · 2007 to 2008
$395k
Development of blood lipid biomarkers for Alzheimer's disease progressionR21AG028754 · NIA · JOHNS HOPKINS UNIVERSITY · PI MIELKE, MICHELLE M · 2007 to 2008
$379k
NIA NIH HHS P50 AG005146NIA NIH HHS P50AG005146NIA NIH HHS R21 AG028754NIA NIH HHS R21AG028754NINDS NIH HHS R21 NS060271NINDS NIH HHS R21NS060271-01
6 · The paper itself

Abstract

The public health burden of Alzheimer disease (AD), the most common neurodegenerative disease, threatens to explode in the middle of this century. Current FDA-approved AD treatments (e.g. cholinesterase inhibitors, NMDA-receptor agonists) do not provide a "cure", but rather a transient alleviation of symptoms for some individuals. Other available therapies are few and of limited effectiveness so additional avenues are needed. Sphingolipid metabolism is a dynamic process that modulates the formation of a number of bioactive metabolites, or second messengers critical in cellular signaling and apoptosis. In brain, the proper balance of sphingolipids is essential for normal neuronal function, as evidenced by a number of severe brain disorders that are the result of deficiencies in enzymes that control sphingolipid metabolism. Laboratory and animals studies suggest both direct and indirect mechanisms by which sphingolipids contribute to amyloid-beta production and Alzheimer pathogenesis but few studies have translated these findings to humans. Building on the laboratory and animal evidence demonstrating the importance of sphingolipid metabolism in AD, this review highlights relevant translational research incorporating and expanding basic findings to humans. A brief biological overview of sphingolipids (sphingomyelins, ceramides, and sulfatides) in AD is first described, followed by a review of human studies including post-mortem studies, clinical and epidemiological studies. Lastly, the potential role of peripheral ceramides in AD pathogenesis is discussed, as well as the possible use of sphingolipids as biomarkers for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersBrainClinical Trials as TopicFemaleHumansSphingolipidstau ProteinsAmyloid beta-PeptidesBiomarkersSphingolipidstau Proteins

Identifiers

PMID20571935
PMCPMC3129545
OpenAlexW2010120002

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.