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Basal forebrain cholinergic dysfunction in Alzheimer's disease--interrelationship with beta-amyloid, inflammation and neurotrophin signaling
Schliebs R.. Neurochemical research, 2005-06-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease, the most common neurodegenerative disorder of senile dementia, is characterized by two major morpho-pathological hallmarks. Deposition of extracellular neuritic, beta-amyloid peptide-containing plaques (senile plaques) in cerebral cortical regions of Alzheimer patients is accompanied by the presence of intracellular neurofibrillary tangles in cerebral pyramidal neurons. Basal forebrain cholinergic dysfunction is also a consistent feature of Alzheimer's disease, which has been suggested to cause, at least partly, the cognitive deficits observed in patients with Alzheimer's disease.
Key findings
- Deposition of extracellular neuritic, beta-amyloid peptide-containing plaques (senile plaques) in cerebral cortical regions of Alzheimer patients is accompanied by the presence of intracellular neurofibrillary tangles in cerebral pyramidal neurons.
- Basal forebrain cholinergic dysfunction is also a consistent feature of Alzheimer's disease, which has been suggested to cause, at least partly, the cognitive deficits observed in patients with Alzheimer's disease.
- Impaired cortical cholinergic neurotransmission may also contribute to beta-amyloid plaque pathology in Alzheimer's disease by affecting expression and processing of the beta-amyloid precursor protein (APP).
- Vice versa, low level of soluble beta-amyloid has been observed to inhibit cholinergic synaptic function.
Why it matters
This review describes basal forebrain cholinergic dysfunction in Alzheimer's disease and its suggested relationship to cognitive deficits, alongside amyloid, inflammation, and neurotrophin signaling. It summarizes mechanisms and does not establish any treatment, cure, or prevention.
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Study details
- Evidence strengthLow
How this study scored 39/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurochemical research) |
| Journal's citation record | 2 / 4 | Neurochemical Research: journal h-index 163 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2005 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 164 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.1 citations a year over 23 year(s) since 2005 |
| Impact for its field and year | 3 / 6 | Cited 5.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 1 / 4 | Cited 14 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Reinhard Schliebs: h-index 47 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Leipzig University: institution h-index 763 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 16187224) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 39 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Schliebs, R. (2005). Basal forebrain cholinergic dysfunction in Alzheimer's disease--interrelationship with beta-amyloid, inflammation and neurotrophin signaling. Neurochemical research. https://doi.org/10.1007/s11064-005-6962-9
Vancouver
Schliebs R. Basal forebrain cholinergic dysfunction in Alzheimer's disease--interrelationship with beta-amyloid, inflammation and neurotrophin signaling. Neurochemical research. 2005. doi:10.1007/s11064-005-6962-9. PMID: 16187224.
BibTeX
@article{schliebs2005-16187224,
author = {Schliebs, R.},
title = {{Basal forebrain cholinergic dysfunction in Alzheimer's disease--interrelationship with beta-amyloid, inflammation and neurotrophin signaling}},
journal = {Neurochemical research},
year = {2005},
doi = {10.1007/s11064-005-6962-9},
pmid = {16187224},
url = {https://doi.org/10.1007/s11064-005-6962-9}
}
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