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43/100

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Disease mechanisms

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

The accumulated evidence on increased levels of inflammatory markers in the cerebrospinal fluid (CSF) of AD patients, along with reports describing CNS alterations caused by senescent immune cells in neuro-degenerative diseases, set out a conceptual framework in which the neuroinflammation hypothesis is being challenged from different angles towards developing new therapies against AD. The current evidence points to controversial findings in the search for therapeutic candidates to treat neuroinflammation in AD. In this article, we discuss a neuroimmune-modulatory perspective for pharmacological exploration of molecular targets against AD, as well as potential deleterious effects of modifying neuroinflammation in the brain parenchyma. We specifically focus on the role of B and T cells, immuno-senescence, the brain lymphatic system (BLS), gut-brain axis alterations, and dysfunctional interactions between neurons, microglia and astrocytes. We also outline a rational framework for identifying "druggable" targets for multi-mechanistic small molecules with therapeutic potential against AD.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Wong-Guerra, M., Calfio, C., Maccioni, R. B., & Rojo, L. E. (2023). Revisiting the neuroinflammation hypothesis in Alzheimer's disease: a focus on the druggability of current targets. Frontiers in pharmacology. https://doi.org/10.3389/fphar.2023.1161850

Vancouver

Wong-Guerra M, Calfio C, Maccioni RB, Rojo LE. Revisiting the neuroinflammation hypothesis in Alzheimer's disease: a focus on the druggability of current targets. Frontiers in pharmacology. 2023. doi:10.3389/fphar.2023.1161850. PMID: 37361208.

BibTeX

@article{wongguerra2023-37361208,
  author  = {Wong-Guerra, M. and Calfio, C. and Maccioni, R. B. and Rojo, L. E.},
  title   = {{Revisiting the neuroinflammation hypothesis in Alzheimer's disease: a focus on the druggability of current targets}},
  journal = {Frontiers in pharmacology},
  year    = {2023},
  doi     = {10.3389/fphar.2023.1161850},
  pmid    = {37361208},
  url     = {https://doi.org/10.3389/fphar.2023.1161850}
}

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How to read this study

Design: this is a narrative review. It summarises a field without a fixed search method, so it shows how authors read the evidence rather than measuring it. Use it to find the primary studies, not as a result in itself.
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 accumulated evidence on increased levels of inflammatory markers in the cerebrospinal fluid (CSF) of AD patients, along with reports describing CNS alterations caused by senescent immune cells in neuro-degenerative diseases, set out a conceptual framework in which the neuroinflammation hypothesis is being challenged from different angles towards developing new therapies against AD.
The current evidence points to controversial findings in the search for therapeutic candidates to treat neuroinflammation in AD.
In this article, we discuss a neuroimmune-modulatory perspective for pharmacological exploration of molecular targets against AD, as well as potential deleterious effects of modifying neuroinflammation in the brain parenchyma.
We specifically focus on the role of B and T cells, immuno-senescence, the brain lymphatic system (BLS), gut-brain axis alterations, and dysfunctional interactions between neurons, microglia and astrocytes.
We also outline a rational framework for identifying "druggable" targets for multi-mechanistic small molecules with therapeutic potential against AD.

Study details

Evidence strengthLow

How this study scored 43/100

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 25 of the 58 points we could judge it on, which is 43 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Frontiers in pharmacology)
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	3 / 5	2023 — within 6 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 37361208)
Free to read	2 / 2	Free to read
Points	25 / 58	Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 25 of the 58 points we could judge it on is 43 out of 100.
Total	43 / 100	—

What each of these 20 components measures, and what this score is not →

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