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36/100

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Treatments

Topic: Brain proteins, microglia and lab models

Plain-language summary

Both of the two most common neurodegenerative disorders, namely Alzheimer's disease (AD) and Parkinson's disease (PD), have multiple lines of evidence from molecular and cellular to epidemiological, that nicotinic transmission is implicated in their pathogenesis. This review article presents evidence of nicotinic acetylcholine receptor (nAChR)-mediated protection against neurotoxicity induced by amyloid-β (Aβ), glutamate, rotenone, and 6-hydroxydopamine (6-OHDA) and the signal transduction involved in this mechanism. Our studies clarified that survival signal transduction, α7 nAChR-Src family-PI3 K-AKT pathway, and subsequent upregulation of Bcl-2 and Bcl-x, would lead to neuroprotection. In addition to the PI3 K-AKT pathway, two other survival pathways, JAK2/STAT3 and MEK/ERK, are proposed by other groups. These three survival pathways are related to each other through intracellular signal transductions in neurons. The JAK2/STAT3 pathway is cholinergic anti-inflammation pathway mediated by α7 nAChR on macrophage and microglia as well as neuron. Recently analyzing the properties of galantamine, we clarify the 4th independent neuroprotective pathway, which is mediated by enhancement of microglial α7 nAChR resulting in upregulation of Aβ phagocytosis. Galantamine sensitizes microglial α7 nAChRs to choline and induce Ca2+ influx into microglia. The Ca2+-induced intracellular signaling cascades may then stimulate Aβ phagocytosis through actin reorganization. The discovery of the 4th pathway would facilitate further investigation of possible nAChRs enhancing drugs targeting not only neuronal but also microglial nAChRs.

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APA 7th

Kawamata, J., & Shimohama, S. (2011). Stimulating nicotinic receptors trigger multiple pathways attenuating cytotoxicity in models of Alzheimer's and Parkinson's diseases. Journal of Alzheimer's disease : JAD. https://doi.org/10.3233/jad-2011-110173

Vancouver

Kawamata J, Shimohama S. Stimulating nicotinic receptors trigger multiple pathways attenuating cytotoxicity in models of Alzheimer's and Parkinson's diseases. Journal of Alzheimer's disease : JAD. 2011. doi:10.3233/jad-2011-110173. PMID: 21403387.

BibTeX

@article{kawamata2011-21403387,
  author  = {Kawamata, J. and Shimohama, S.},
  title   = {{Stimulating nicotinic receptors trigger multiple pathways attenuating cytotoxicity in models of Alzheimer's and Parkinson's diseases}},
  journal = {Journal of Alzheimer's disease : JAD},
  year    = {2011},
  doi     = {10.3233/jad-2011-110173},
  pmid    = {21403387},
  url     = {https://doi.org/10.3233/jad-2011-110173}
}

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How to read this study

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Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

The JAK2/STAT3 pathway is cholinergic anti-inflammation pathway mediated by α7 nAChR on macrophage and microglia as well as neuron.
Recently analyzing the properties of galantamine, we clarify the 4th independent neuroprotective pathway, which is mediated by enhancement of microglial α7 nAChR resulting in upregulation of Aβ phagocytosis.
Galantamine sensitizes microglial α7 nAChRs to choline and induce Ca2+ influx into microglia.
The Ca2+-induced intracellular signaling cascades may then stimulate Aβ phagocytosis through actin reorganization.
The discovery of the 4th pathway would facilitate further investigation of possible nAChRs enhancing drugs targeting not only neuronal but also microglial nAChRs.

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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 (Journal of Alzheimer's disease : JAD)
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	2011 — 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 21403387)
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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