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Neuropharmacology of Alzheimer Disease
Bhumika Satdive*, Shweta Padosa, Yashodeep Patil. Zenodo (CERN European Organization for Nuclear Research), 2025-11-25
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by memory loss, cognitive decline, and behavioral changes. The disease develops through several mechanisms, including amyloid-beta plaque formation, tau protein hyperphosphorylation, oxidative stress, inflammation, and synaptic failure. Neuropharmacological treatments aim to influence these processes to relieve symptoms and slow disease progression. Current drugs mainly include cholinesterase inhibitors, which strengthen cholinergic activity, and NMDA receptor antagonists, which balance glutamatergic transmission. New therapeutic directions focus on disease modification by targeting amyloid and tau pathology, oxidative stress, and neuroinflammatory pathways. Advances in molecular neuropharmacology — such as monoclonal antibodies, small-molecule inhibitors, and neuroprotective compounds — may lead to more effective therapies. Understanding the complex molecular and neurochemical basis of AD is essential for developing next-generation drugs to enhance cognitive health and quality of life.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Satdive, B., Padosa, S., & Patil, Y. (2025). Neuropharmacology of Alzheimer Disease. Zenodo (CERN European Organization for Nuclear Research). https://doi.org/10.5281/zenodo.17711756
Vancouver
Satdive B, Padosa S, Patil Y. Neuropharmacology of Alzheimer Disease. Zenodo (CERN European Organization for Nuclear Research). 2025. doi:10.5281/zenodo.17711756.
BibTeX
@article{satdive2025-92336d40,
author = {Satdive, Bhumika and Padosa, Shweta and Patil, Yashodeep},
title = {{Neuropharmacology of Alzheimer Disease}},
journal = {Zenodo (CERN European Organization for Nuclear Research)},
year = {2025},
doi = {10.5281/zenodo.17711756},
url = {https://doi.org/10.5281/zenodo.17711756}
}
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
- Neuropharmacological treatments aim to influence these processes to relieve symptoms and slow disease progression.
- Current drugs mainly include cholinesterase inhibitors, which strengthen cholinergic activity, and NMDA receptor antagonists, which balance glutamatergic transmission.
- New therapeutic directions focus on disease modification by targeting amyloid and tau pathology, oxidative stress, and neuroinflammatory pathways.
- Advances in molecular neuropharmacology — such as monoclonal antibodies, small-molecule inhibitors, and neuroprotective compounds — may lead to more effective therapies.
- Understanding the complex molecular and neurochemical basis of AD is essential for developing next-generation drugs to enhance cognitive health and quality of life.
Why it matters
Current neuropharmacological treatments for Alzheimer's disease mainly include cholinesterase inhibitors and NMDA receptor antagonists, which aim to relieve symptoms and slow disease progression. New directions focus on disease modification by targeting amyloid and tau pathology, oxidative stress and neuroinflammatory pathways, with monoclonal antibodies and small-molecule inhibitors as possible future therapies.
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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 randomized / blinded because the record does not state it. We have no data on journal's citation record, senior author's track record and institution's track record, so those were left out: it earned 25 of the 89 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) |
| Randomized / blinded | 0 / 2 | No randomization 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 | 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 | 0 / 3 | OpenAlex lists 0 institution(s) in 0 countries — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 2 / 2 | Free to read |
| Points | 25 / 89 | Scored on 17 of 20 parts. We have no data for the rest, so they are left out: 25 of the 89 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
- DOI: 10.5281/zenodo.17711756
- Original source →
- Free full text: Zenodo (CERN European Organization for Nuclear Research) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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