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Common Dysregulated Pathways and Genes in Alzheimer’s, Parkinson’s, and Huntington’s Diseases: A Computational Analysis to Nominate Candidate Gene Targets for Drug Repurposing
Abdelsalam NA, Elsadany M, Badr E.. bioRxiv, 2026-07-25
Topic: Gut, metabolism and diet
Neurodegenerative diseases are a major threat to older adults and represent a growing global health burden as the elderly population continues to expand. The complexity of neurodegenerative diseases and the incomplete understanding of their pathophysiology limit the development of effective therapeutics. To study common neurodegenerative mechanisms and accordingly potential drug targets across Alzheimer’s, Parkinson’s, and Huntington’s diseases, transcriptomic profiles of patients with each disease were analyzed to detect common differentially expressed genes and common enriched pathways. Common differentially expressed genes involved in the shared pathways were identified as key drug targets and validated in silico to study the impact of their dysregulation. Three pathways were enriched and upregulated across the three diseases, along with 274 common differentially expressed genes. Two of the shared pathways were involved in activation of the transcription factor nuclear factor kappa B (NF-κB), indicating inflammatory signaling. The third pathway involved regulation of BCL2L11 transcription by RUNX3, which contributes to the protective effect of neurodegenerative diseases against cancer. Five key drug targets were identified: NFKBIA , NFKB1 , RELA , TRIM4 , and SMAD4 . They were significantly upregulated across all three diseases and involved in the shared pathways. Drugs that target the expression of these genes and previously approved by Food and Drug Administration were reported for treatment repurposing for the three neurodegenerative diseases. The resultant drug list included the conventional and commonly safe antihyperlipidemics, antihypertensives, antidiabetics, analgesics, diuretics, antiparkinson’s, and antipsychotics.
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APA 7th
Abdelsalam, N. A., Elsadany, M., & Badr, E. (2026). Common Dysregulated Pathways and Genes in Alzheimer’s, Parkinson’s, and Huntington’s Diseases: A Computational Analysis to Nominate Candidate Gene Targets for Drug Repurposing. bioRxiv. https://doi.org/10.64898/2026.07.22.739294
Vancouver
Abdelsalam NA, Elsadany M, Badr E. Common Dysregulated Pathways and Genes in Alzheimer’s, Parkinson’s, and Huntington’s Diseases: A Computational Analysis to Nominate Candidate Gene Targets for Drug Repurposing. bioRxiv. 2026. doi:10.64898/2026.07.22.739294.
BibTeX
@article{abdelsalam2026-dfc076bf,
author = {Abdelsalam, N. A. and Elsadany, M. and Badr, E.},
title = {{Common Dysregulated Pathways and Genes in Alzheimer’s, Parkinson’s, and Huntington’s Diseases: A Computational Analysis to Nominate Candidate Gene Targets for Drug Repurposing}},
journal = {bioRxiv},
year = {2026},
doi = {10.64898/2026.07.22.739294},
url = {https://doi.org/10.64898/2026.07.22.739294}
}
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Key findings
- They were significantly upregulated across all three diseases and involved in the shared pathways.
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Study details
- Evidence strengthLow
How this study scored 16/100
Preprint — not yet peer-reviewed. It scored 21 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. 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 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 multi-centre collaboration, so those were left out: it earned 13 of the 62 points we could judge it on, which is 21 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (bioRxiv) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| 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 | 4 / 10 | Preprint — not yet peer-reviewed. Hosted on a preprint server. |
| How recent | 5 / 5 | 2026 — within 1 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 | — / 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 |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 13 / 62 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 13 of the 62 points we could judge it on is 21 out of 100. |
| Total | 21 / 100 | Capped to 16 because this is not a peer-reviewed article. |
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