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Neurobiological and therapeutic landmarks of depression associated with Alzheimer’s disease dementia
Ilinca Untu, Michael Davidson, Gabriela Dumitriţa Stanciu, Jonathan Rabinowitz, Romeo Dobrin, Diana Sabina Vieru, Bogdan-Ionel Tamba. Frontiers in Aging Neuroscience, 2025-06-02
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Depression in Alzheimer's disease (AD) dementia has become an increasingly recognized public health concern due to its high prevalence and substantial impact on patient outcomes. Despite extensive research having been conducted over the past decades, the precise causal mechanisms and the nature of the relationship between depression and AD dementia remain incompletely understood. This narrative review examines the bidirectional interaction between depression and Alzheimer's disease, emphasizing shared neurobiological pathways, including neurotransmitter dysregulation, neuroinflammation, abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis, and deficits in neuroplasticity. These mechanisms likely contribute to the acceleration of neurodegeneration in AD and the onset or worsening of depressive symptoms. Current therapeutic approaches remain largely nonspecific, with a lack of targeted therapies that address the unique pathophysiological context of depression in AD. While progress has been made, key research gaps remain, particularly in understanding the complex biological interactions between these two conditions. Future research should focus on identifying specific biomarkers and developing personalized treatment strategies tailored to the neurobiological features of both depression and AD. By addressing these neurobiological mechanisms, we can develop more effective and targeted interventions, ultimately improving patient outcomes and advancing clinical care for this dual pathology.
What this study adds
Evidence grade: Low
This is a narrative review. This review describes shared biological pathways between depression and Alzheimer's dementia and notes that current treatments are largely nonspecific. It highlights gaps in understanding and the need for targeted, personalized approaches rather than reporting a new therapy.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Untu, I., Davidson, M., Stanciu, G. D., Rabinowitz, J., Dobrin, R., Vieru, D. S., et al. (2025). Neurobiological and therapeutic landmarks of depression associated with Alzheimer’s disease dementia. Frontiers in Aging Neuroscience. https://doi.org/10.3389/fnagi.2025.1584607
Vancouver
Untu I, Davidson M, Stanciu GD, Rabinowitz J, Dobrin R, Vieru DS, et al. Neurobiological and therapeutic landmarks of depression associated with Alzheimer’s disease dementia. Frontiers in Aging Neuroscience. 2025. doi:10.3389/fnagi.2025.1584607. PMID: 40529210.
BibTeX
@article{untu2025-40529210,
author = {Untu, Ilinca and Davidson, Michael and Stanciu, Gabriela Dumitriţa and Rabinowitz, Jonathan and Dobrin, Romeo and Vieru, Diana Sabina and Tamba, Bogdan-Ionel},
title = {{Neurobiological and therapeutic landmarks of depression associated with Alzheimer’s disease dementia}},
journal = {Frontiers in Aging Neuroscience},
year = {2025},
doi = {10.3389/fnagi.2025.1584607},
pmid = {40529210},
url = {https://doi.org/10.3389/fnagi.2025.1584607}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- These mechanisms likely contribute to the acceleration of neurodegeneration in AD and the onset or worsening of depressive symptoms.
- Current therapeutic approaches remain largely nonspecific, with a lack of targeted therapies that address the unique pathophysiological context of depression in AD.
- While progress has been made, key research gaps remain, particularly in understanding the complex biological interactions between these two conditions.
- Future research should focus on identifying specific biomarkers and developing personalized treatment strategies tailored to the neurobiological features of both depression and AD.
- By addressing these neurobiological mechanisms, we can develop more effective and targeted interventions, ultimately improving patient outcomes and advancing clinical care for this dual pathology.
Why it matters
This review describes shared biological pathways between depression and Alzheimer's dementia and notes that current treatments are largely nonspecific. It highlights gaps in understanding and the need for targeted, personalized approaches rather than reporting a new therapy.
Study details
- Study designnarrative review
- Evidence strengthLow
How this study scored 39/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in Aging Neuroscience) |
| Journal's citation record | 2 / 4 | Frontiers in Aging Neuroscience: journal h-index 174 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | Design recorded as “narrative review”, which our rubric does not rank (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 | 2 / 7 | Cited 9 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 5.7× 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 9 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Bogdan-Ionel Tamba: h-index 28 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Bar-Ilan University: institution h-index 553 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40529210) |
| Free to read | 2 / 2 | Free to read |
| Total | 39 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fnagi.2025.1584607
- PubMed: 40529210
- Original source →
- Free full text: Frontiers in Aging Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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