Evidence map›Paper›PMID 10885540›Full record

ReviewMetabolic brain disease2000

The cholinergic neuronal phenotype in Alzheimer's disease.

J K Blusztajn, B Berse

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Isolation of Fucoxanthin fromBiomedicines · 2023
    Article
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  13. Review
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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

2 authors at 1 institution in 1 country.

J K BlusztajnDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, MA 02118, USA. jbluszta@bu.edu
B Berse
Boston University · US

Funding

TIME FRAMES OF CHOLINE ENHANCEMENT OF MEMORYP01AG009525 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BLUSZTAJN, JAN KRZYSZTOF · 1991 to 2010
$11.8M
NIA NIH HHS AG09525
6 · The paper itself

Abstract

The synthesis, storage and release of acetylcholine (ACh) requires the expression of several specialized proteins, including choline acetyltransferase (ChAT) and the vesicular ACh transporter (VAChT). The VAChT gene is located within the first intron of the ChAT gene. This unique genomic organization permits coordinated activation of expression of the two genes by extracellular factors. Much less is known about factors that reduce the expression of the cholinergic phenotype. A cholinergic deficit is one of the primary features of Alzheimer's disease (AD), and AD brains are characterized by amyloid deposits composed primarily of A beta peptides. Although A beta peptides are neurotoxic, part of the cholinergic deficit in AD could be attributed to the suppression of cholinergic markers in the absence of cell death. Indeed, we and others demonstrated that synthetic A beta peptides, at submicromolar concentrations that cause no cytotoxicity, reduce the expression of cholinergic markers in neuronal cells. Another feature of AD is abnormal phospholipid turnover, which might be related to the progressive accumulation of apolipoprotein E (apoE) within amyloid plaques, leading perhaps to the reduction of apoE content in the CSF of AD patients. ApoE is a component of very low density lipoproteins (VLDL). As a first step in investigating a potential neuroprotective function of apoE, we determined the effects of VLDL on ACh content in neuronal cells. We found that VLDL increases ACh levels, and that it can partially offset the anticholinergic actions of A beta peptides.

Indexed as

Membrane Transport ProteinsVesicular Transport ProteinsAcetylcholineAlzheimer DiseaseCarrier ProteinsCholine O-AcetyltransferaseChromosome MappingHumansNeuronsPhenotypeVesicular Acetylcholine Transport ProteinsAcetylcholineCarrier ProteinsCholine O-AcetyltransferaseMembrane Transport ProteinsSLC18A3 protein, humanVesicular Acetylcholine Transport ProteinsVesicular Transport Proteins

Identifiers

PMID10885540
OpenAlexW2056439017

What OpenQuestion holds

Textmetadata
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.