Evidence map›Paper›PMID 33867926›Full record

ReviewFrontiers in neuroscience2021

Sialometabolism in Brain Health and Alzheimer's Disease.

Punam Rawal, Liqin Zhao

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Metabolic Brain Disorders: Prodromes, Symptoms, and Syndromes.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
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  11. Review
  12. Review
  13. Article
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  15. Review
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  17. Review
  18. Article
  19. Enhanced Detection of ChargedAnalytical chemistry · 2023
    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

2 authors at 1 institution in 1 country.

Punam RawalDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, KS, United States.
Liqin ZhaoDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, KS, United States.
University of Kansas · US

Funding

Reshaping ApoE4 and Alzheimer's Brains with ApoE2R01AG071682 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI TERUNA J. SIAHAAN, Liqin Zhao · 2022 to 2026
$3.4M
Sporadic Alzheimer's Disease: A Bioenergetic Etiology?R01AG061038 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI ZHAO, LIQIN · 2019 to 2023
$1.9M
NIA NIH HHS R01 AG061038NIA NIH HHS R01 AG071682
6 · The paper itself

Abstract

Sialic acids refer to a unique family of acidic sugars with a 9-carbon backbone that are mostly found as terminal residues in glycan structures of glycoconjugates including both glycoproteins and glycolipids. The highest levels of sialic acids are expressed in the brain where they regulate neuronal sprouting and plasticity, axon myelination and myelin stability, as well as remodeling of mature neuronal connections. Moreover, sialic acids are the sole ligands for microglial Siglecs (sialic acid-binding immunoglobulin-type lectins), and sialic acid-Siglec interactions have been indicated to play a critical role in the regulation of microglial homeostasis in a healthy brain. The recent discovery of CD33, a microglial Siglec, as a novel genetic risk factor for late-onset Alzheimer's disease (AD), highlights the potential role of sialic acids in the development of microglial dysfunction and neuroinflammation in AD. Apart from microglia, sialic acids have been found to be involved in several other major changes associated with AD. Elevated levels of serum sialic acids have been reported in AD patients. Alterations in ganglioside (major sialic acid carrier) metabolism have been demonstrated as an aggravating factor in the formation of amyloid pathology in AD. Polysialic acids are linear homopolymers of sialic acids and have been implicated to be an important regulator of neurogenesis that contributes to neuronal repair and recovery from neurodegeneration such as in AD. In summary, this article reviews current understanding of neural functions of sialic acids and alterations of sialometabolism in aging and AD brains. Furthermore, we discuss the possibility of looking at sialic acids as a promising novel therapeutic target for AD intervention.

Indexed as

CD33gangliosidelate-onset Alzheimer’s diseaseneural cell adhesion moleculePSA-NCAMsialic acidsialylationSiglec

Identifiers

PMID33867926
PMCPMC8044809
OpenAlexW3140243968

What Socratic holds

Textmetadata
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 Socratic graph.