Evidence map›Paper›PMID 15644984›Full record

ReviewJournal of psychiatry & neuroscience : JPN2004

Interactions between beta-amyloid and central cholinergic neurons: implications for Alzheimer's disease.

Satyabrata Kar, Stephen P M Slowikowski, David Westaway, Howard T J Mount

Open access · greenAbstract readReview
In one paragraph

Review in Journal of psychiatry & neuroscience : JPN, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% 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

137 citing papers in PubMed, 1 synthesis or guideline pooled it, 349 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Reduction in hippocampal cholinergic neurostimulating peptide enhances memory impairment in AppAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Article
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  11. Reduction in [Brain research · 2025
    Article
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  18. Copper-mediated neurotoxicity and genetic vulnerability in the background of neurodegenerative diseases in C. elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
  19. Article
  20. Investigating the Potential of Essential Oils fromPlants (Basel, Switzerland) · 2024
    Article

77 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

4 authors at 2 institutions in 1 country.

Satyabrata KarDepartment of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada. skar@ualberta.ca
Stephen P M Slowikowski
David Westaway
Howard T J Mount
Occupational Cancer Research Centre · CAUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is an age-related neurodegenerative disorder that is characterized by a progressive loss of memory and deterioration of higher cognitive functions. The brain of an individual with Alzheimer's disease exhibits extracellular plaques of aggregated beta-amyloid protein (Abeta), intracellular neurofibrillary tangles that contain hyperphosphorylated tau protein and a profound loss of basal forebrain cholinergic neurons that innervate the hippocampus and the neocortex. Abeta accumulation may trigger or contribute to the process of neurodegeneration. However, the mechanisms whereby Abeta induces basal forebrain cholinergic cell loss and cognitive impairment remain obscure. Physiologically relevant concentrations of Abeta-related peptides have acute, negative effects on multiple aspects of acetylcholine (ACh) synthesis and release, without inducing toxicity. These data suggest a neuromodulatory influence of the peptides on central cholinergic functions. Long-term exposure to micromolar Abeta induces cholinergic cell toxicity, possibly via hyperphosphorylation of tau protein. Conversely, activation of selected cholinergic receptors has been shown to alter the processing of the amyloid precursor protein as well as phosphorylation of tau protein. A direct interaction between Abeta and nicotinic ACh receptors has also been demonstrated. This review addresses the role of Abeta-related peptides in regulating the function and survival of central cholinergic neurons and the relevance of these effects to cholinergic deficits in Alzheimer's disease. Understanding the functional interrelations between Abeta peptides, cholinergic neurons and tau phosphorylation will unravel the biologic events that precede neurodegeneration and may lead to the development of more effective pharmacotherapies for Alzheimer's disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainCell DeathCholinergic FibersHumansNeurofibrillary TanglesNeuronsPeptide FragmentsPhosphorylationReceptors, Cholinergictau ProteinsAmyloid beta-PeptidesPeptide FragmentsReceptors, Cholinergictau Proteins

Identifiers

PMID15644984
PMCPMC524960
OpenAlexW2140190457

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.