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Structure-function implications in Alzheimer's disease: effect of Abeta oligomers at central synapses
Cerpa W, Dinamarca MC, Inestrosa NC.. Current Alzheimer research, 2008-06-01
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Alzheimer's disease (AD) is the most prevalent neurodegenerative disease in the growing population of elderly people. A characteristic of AD is the accumulation of plaques in the brain of AD patients, and theses plaques mainly consist of aggregates of amyloid beta-peptide (Abeta). All converging lines of evidence suggest that progressive accumulation of the Abeta plays a central role in the genesis of Alzheimer's disease and it was long understood that Abeta had to be assembled into extracellular amyloid fibrils to exert its cytotoxic effects. This process could be modulated by molecular chaperones which inhibit or accelerate the amyloid formation. The enzyme Acetylcholinesterase (AChE) induces Abeta fibrils formation, forming a stable complex highly neurotoxic. On the other hand, laminin inhibit the Abeta fibrils formation and depolymerizate Abeta fibrils also. Over the past decade, data have emerged from the use of several sources of Abeta (synthetic, cell culture, transgenic mice and human brain) to suggest that intermediate species called Abeta oligomers are also injurious. Accumulating evidence suggests that soluble forms of Abeta are indeed the proximate effectors of synapse loss and neuronal injury. On the other hand, the member of the Wnt signaling pathway, beta-catenin was markedly reduced in AD patients carrying autosomal dominant PS-1. Also, neurons incubated with Abeta revealed a significant dose-dependent decrease in the levels of cytosolic beta-catenin an effect which was reversed in cells co-incubated with increasing concentrations of lithium, an activator of Wnt signaling pathway. Wnt signaling blocks the behavioural impairments induced by hippocampal injection of Abeta, therefore the activation of Wnt signaling protects against the Abeta neurotoxicity. Here we review recent progress about Abeta structure and function, from the formation of amyloid fibrils and some molecular chaperones which modulate the amyloidogenesic process to synaptic damage induce by Abeta oligomers.
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APA 7th
Cerpa, W., Dinamarca, M. C., & Inestrosa, N. C. (2008). Structure-function implications in Alzheimer's disease: effect of Abeta oligomers at central synapses. Current Alzheimer research. https://doi.org/10.2174/156720508784533321
Vancouver
Cerpa W, Dinamarca MC, Inestrosa NC. Structure-function implications in Alzheimer's disease: effect of Abeta oligomers at central synapses. Current Alzheimer research. 2008. doi:10.2174/156720508784533321. PMID: 18537540.
BibTeX
@article{cerpa2008-18537540,
author = {Cerpa, W. and Dinamarca, M. C. and Inestrosa, N. C.},
title = {{Structure-function implications in Alzheimer's disease: effect of Abeta oligomers at central synapses}},
journal = {Current Alzheimer research},
year = {2008},
doi = {10.2174/156720508784533321},
pmid = {18537540},
url = {https://doi.org/10.2174/156720508784533321}
}
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Key findings
- All converging lines of evidence suggest that progressive accumulation of the Abeta plays a central role in the genesis of Alzheimer's disease and it was long understood that Abeta had to be assembled into extracellular amyloid fibrils to exert its cytotoxic effects.
- Over the past decade, data have emerged from the use of several sources of Abeta (synthetic, cell culture, transgenic mice and human brain) to suggest that intermediate species called Abeta oligomers are also injurious.
- Accumulating evidence suggests that soluble forms of Abeta are indeed the proximate effectors of synapse loss and neuronal injury.
- Also, neurons incubated with Abeta revealed a significant dose-dependent decrease in the levels of cytosolic beta-catenin an effect which was reversed in cells co-incubated with increasing concentrations of lithium, an activator of Wnt signaling pathway.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Current Alzheimer research) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2008 — within 20 year(s) of the newest study here |
| 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 18537540) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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