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Comprehensive Review on Alzheimer Disease: Causes, Risk Factors, Pathology, Mechanisms
Bhakti More*, Navnath Bendke, Pratiksha Swami, Sharmin Shaikh, Dr. Ganesh Talsarwad. Zenodo (CERN European Organization for Nuclear Research), 2026-02-06
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer’s disease (AD) is the most widespread neurodegenerative disorder and a leading cause of dementia seen in clinical practice. Although many therapeutic strategies have been explored, AD continues to present a major challenge for healthcare systems around the world. This article begins by summarizing the key biological processes that lead to neuronal damage in AD. It then critically examines important research on current pharmacological treatments and highlights recent innovations and developing therapies. The review covers the main characteristics, classification, FDA approval status, mechanisms of action, therapeutic benefits, and common adverse effects of both established and emerging drugs for AD management. Traditional drug classes discussed include cholinesterase inhibitors, monoclonal antibodies, and other therapies such as memantine, valproic acid, and rosiglitazone. The article also explores newer monoclonal antibodies—donanemab, gantenerumab, solanezumab, bapineuzumab, crenezumab, and semorinemab—and evaluates nutritional supplements like vitamin E (alpha-tocopherol) and caprylidene. Additional agents that target tau and amyloid pathways, such as methylthioninium (MT), leuco-methylthioninium bis (LMTM), and tramiprosate, are reviewed for their ability to inhibit Aβ aggregation. The discussion extends to antidiabetic and anti-inflammatory drugs recently proposed for AD therapy. These include NE3107, a compound with anti-inflammatory and insulin-sensitizing effects, and the commonly used antidiabetic drug metformin. Anti-neuroinflammatory agents— such as sodium oligomannate (GV-971), intravenous immunoglobulin infusions to reduce circulating Aβ components, and masitinib, a tyrosine kinase inhibitor affecting mast cells and microglia—are also highlighted.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
More, B., Bendke, N., Swami, P., Shaikh, S., & Talsarwad, D. G. (2026). Comprehensive Review on Alzheimer Disease: Causes, Risk Factors, Pathology, Mechanisms. Zenodo (CERN European Organization for Nuclear Research). https://doi.org/10.5281/zenodo.18509183
Vancouver
More B, Bendke N, Swami P, Shaikh S, Talsarwad DG. Comprehensive Review on Alzheimer Disease: Causes, Risk Factors, Pathology, Mechanisms. Zenodo (CERN European Organization for Nuclear Research). 2026. doi:10.5281/zenodo.18509183.
BibTeX
@article{more2026-54d0f1d7,
author = {More, Bhakti and Bendke, Navnath and Swami, Pratiksha and Shaikh, Sharmin and Talsarwad, Dr. Ganesh},
title = {{Comprehensive Review on Alzheimer Disease: Causes, Risk Factors, Pathology, Mechanisms}},
journal = {Zenodo (CERN European Organization for Nuclear Research)},
year = {2026},
doi = {10.5281/zenodo.18509183},
url = {https://doi.org/10.5281/zenodo.18509183}
}
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.
Key findings
- The article also explores newer monoclonal antibodies—donanemab, gantenerumab, solanezumab, bapineuzumab, crenezumab, and semorinemab—and evaluates nutritional supplements like vitamin E (alpha-tocopherol) and caprylidene.
- Additional agents that target tau and amyloid pathways, such as methylthioninium (MT), leuco-methylthioninium bis (LMTM), and tramiprosate, are reviewed for their ability to inhibit Aβ aggregation.
- The discussion extends to antidiabetic and anti-inflammatory drugs recently proposed for AD therapy.
- These include NE3107, a compound with anti-inflammatory and insulin-sensitizing effects, and the commonly used antidiabetic drug metformin.
- Anti-neuroinflammatory agents— such as sodium oligomannate (GV-971), intravenous immunoglobulin infusions to reduce circulating Aβ components, and masitinib, a tyrosine kinase inhibitor affecting mast cells and microglia—are also highlighted.
Why it matters
This review covers established and emerging Alzheimer's drugs, including cholinesterase inhibitors, memantine, several monoclonal antibodies, nutritional supplements, and agents targeting tau and amyloid pathways. It is a summary of existing research rather than a new trial, so it does not by itself show that any treatment cures or prevents the disease.
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Study details
- Evidence strengthLow
How this study scored 41/100
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, times cited, citations per year, impact for its field and year, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 26 of the 64 points we could judge it on, which is 41 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 | 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 | 0 / 6 | No other study in this library cites it |
| 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 | 2 / 2 | Free to read |
| Points | 26 / 64 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 26 of the 64 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
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