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28/100

✓ Peer-reviewed alzhub usefulness score 28 out of 100. Risk genes beyond APOE

Topic: Amyloid, tau and blood-test diagnosis

The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary. Results:CRISPR/Cas9 gene editing in genes associated with AD, APP, PSEN1, BACE1, and APOE4 was very effective in mitigating β-amyloid deposition, decreasing tau hyperphosphorylation, and improving neuronal function in vivo and in vitro. Efficient delivery through viral and non-viral vectors demonstrated precise gene modification with low off-targeting, with high specificity reported in neuronal cells. Studies on functional outcomes in animal models of AD showed improved learning and memory performance, which was associated with reduced amyloid plaque burden and neuroinflammation. These findings demonstrate not only that CRISPR/Cas9 affects core pathogenic pathways but also that it is translatable to measurable cognitive enhancement, an indication of potential as a disease-modifying therapy.

Key findings

The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary.
Results:CRISPR/Cas9 gene editing in genes associated with AD, APP, PSEN1, BACE1, and APOE4 was very effective in mitigating β-amyloid deposition, decreasing tau hyperphosphorylation, and improving neuronal function in vivo and in vitro.
Efficient delivery through viral and non-viral vectors demonstrated precise gene modification with low off-targeting, with high specificity reported in neuronal cells.
Studies on functional outcomes in animal models of AD showed improved learning and memory performance, which was associated with reduced amyloid plaque burden and neuroinflammation.
These findings demonstrate not only that CRISPR/Cas9 affects core pathogenic pathways but also that it is translatable to measurable cognitive enhancement, an indication of potential as a disease-modifying therapy.

Why it matters

This hypothetical framework reports that CRISPR/Cas9 editing of APP, PSEN1, BACE1 and APOE4 reduced β-amyloid deposition, decreased tau hyperphosphorylation and improved learning and memory in animal models. It is a proposed therapeutic framework, not an established treatment for people.

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Study details

Evidence strengthLow

How this study scored 28/100

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. We have no data on journal's citation record and senior author's track record, so those were left out: it earned 26 of the 92 points we could judge it on, which is 28 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Zenodo (CERN European Organization for Nuclear 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	4 / 5	2025 — within 3 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)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	0 / 7	Cited 0 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.0 citations a year over 3 year(s) since 2025
Impact for its field and year	0 / 6	Cited 0.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	0 / 6	No other study in this library cites it
Still being cited	0 / 4	Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	— / 4	OpenAlex's profile for last-listed author Abdul Kalam Azad holds only 1 work(s), too few to judge a track record — left out of this score
Institution's track record	0 / 3	Jagannath University: institution h-index 116 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 2 countries
Indexed in PubMed	1 / 2	Not in PubMed, but has a DOI
Free to read	2 / 2	Free to read
Points	26 / 92	Scored on 18 of 20 parts. We have no data for the rest, so they are left out: 26 of the 92 points we could judge it on is 28 out of 100.
Total	28 / 100	—

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

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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

Karim, M. A., Meem, S. P., & Azad, A. K. (2025). CRISPR–Cas9–Mediated Genetic Correction for Alzheimer's Disease A Hypothetical Therapeutic Framework. Zenodo (CERN European Organization for Nuclear Research). https://doi.org/10.5281/zenodo.18032007

Vancouver

Karim MA, Meem SP, Azad AK. CRISPR–Cas9–Mediated Genetic Correction for Alzheimer's Disease A Hypothetical Therapeutic Framework. Zenodo (CERN European Organization for Nuclear Research). 2025. doi:10.5281/zenodo.18032007.

BibTeX

@article{karim2025-8dfd48d1,
  author  = {Karim, Md Asif and Meem, Sohana Parveen and Azad, Abdul Kalam},
  title   = {{CRISPR–Cas9–Mediated Genetic Correction for Alzheimer's Disease A Hypothetical Therapeutic Framework}},
  journal = {Zenodo (CERN European Organization for Nuclear Research)},
  year    = {2025},
  doi     = {10.5281/zenodo.18032007},
  url     = {https://doi.org/10.5281/zenodo.18032007}
}

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