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Targeting Inflammation in Alzheimer’s Disease: Insights Into Pathophysiology and Therapeutic Avenues-A Comprehensive Review
Vasileios Topalis, Charalampos Voros, Mairi Ziaka. Journal of Geriatric Psychiatry and Neurology, 2025-07-23
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's Disease (AD) is the most common dementia, affecting mainly older adults, particularly over 65. Characterized by progressive cognitive decline-including deficits in memory, executive functions, and language, alongside behavioral disturbances-AD arises from complex pathophysiological mechanisms. These include neurotransmitter imbalances, cholinergic deficits, amyloid-beta (Aβ) toxicity, tau protein hyperphosphorylation, oxidative stress, synaptic dysfunction, and neuroinflammatory processes. Growing evidence highlights the protective role of microglia in AD pathology through their immune functions, phagocytic clearance of Aβ proteins, and trophic support to promote tissue repair and maintain cerebral homeostasis, as alterations in their response to Aβ are linked to an increased risk of AD. However, disruptions in homeostasis or tissue alterations may trigger microglial activation, leading to detrimental effects such as increased inflammatory activity, impaired microglial-mediated clearance, synapse loss, and neuronal damage. Astrocytes, a distinct type of glial cell with homeostatic functions, also exhibit neuroprotective effects. However, the presence of Aβ may result in astrocyte reactivity, leading to neurotoxic effects associated with disturbances of calcium levels, activation of proinflammatory pathways, gliotransmission, altered tau metabolism, and impaired clearance of Aβ. Despite substantial research, AD remains challenging to diagnose early and lacks effective treatments. Given its multifactorial nature, therapeutic approaches primarily aim to slow progression and remain limited in achieving a definitive cure. While most current strategies focus on mitigating the toxic effects of Aβ and tau proteins, growing interest has emerged in addressing neuroinflammation as a potential means to delay or prevent neurodegeneration. Targeting neuroinflammation could open new therapeutic avenues for the treatment of AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Topalis, V., Voros, C., & Ziaka, M. (2025). Targeting Inflammation in Alzheimer’s Disease: Insights Into Pathophysiology and Therapeutic Avenues-A Comprehensive Review. Journal of Geriatric Psychiatry and Neurology. https://doi.org/10.1177/08919887251361578
Vancouver
Topalis V, Voros C, Ziaka M. Targeting Inflammation in Alzheimer’s Disease: Insights Into Pathophysiology and Therapeutic Avenues-A Comprehensive Review. Journal of Geriatric Psychiatry and Neurology. 2025. doi:10.1177/08919887251361578. PMID: 40698455.
BibTeX
@article{topalis2025-40698455,
author = {Topalis, Vasileios and Voros, Charalampos and Ziaka, Mairi},
title = {{Targeting Inflammation in Alzheimer’s Disease: Insights Into Pathophysiology and Therapeutic Avenues-A Comprehensive Review}},
journal = {Journal of Geriatric Psychiatry and Neurology},
year = {2025},
doi = {10.1177/08919887251361578},
pmid = {40698455},
url = {https://doi.org/10.1177/08919887251361578}
}
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
- Growing evidence highlights the protective role of microglia in AD pathology through their immune functions, phagocytic clearance of Aβ proteins, and trophic support to promote tissue repair and maintain cerebral homeostasis, as alterations in their response to Aβ are linked to an increased risk of AD.
- However, the presence of Aβ may result in astrocyte reactivity, leading to neurotoxic effects associated with disturbances of calcium levels, activation of proinflammatory pathways, gliotransmission, altered tau metabolism, and impaired clearance of Aβ.
Why it matters
This review describes how microglia can protect against Alzheimer's by clearing amyloid-beta, but that disrupted homeostasis can trigger harmful microglial activation, inflammation, synapse loss and neuronal damage. It frames inflammation as a possible therapeutic avenue but reports no tested treatment or outcome.
Study details
- Evidence strengthLow
How this study scored 37/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of Geriatric Psychiatry and Neurology) |
| Journal's citation record | 1 / 4 | Journal of Geriatric Psychiatry and Neurology: journal h-index 105 (OpenAlex, 2026-10-29) |
| 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 | 2 / 7 | Cited 10 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.3 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 3.1× 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 | 1 / 4 | Cited 10 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Mairi Ziaka: h-index 15 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Bern: institution h-index 977 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40698455) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 37 / 100 | — |
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