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Targeting Metabolic Dysregulation in Alzheimer’s Disease: A Potential Therapeutic Strategy
Nivedita Barnwal, Sonal Dubey, Prashant Kumar Tiwari. Current Drug Metabolism, 2025-09-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD), the most common form of dementia, is characterized by progressive cognitive decline and neuropathological hallmarks, including amyloid-beta plaques and tau tangles. Emerging evidence implicates metabolic dysfunction as a critical contributor to the pathogenesis and progression of AD. Impaired glucose metabolism, mitochondrial dysfunction, oxidative stress, and lipid dysregulation are frequently observed in AD brains, suggesting that metabolic dysfunction may exacerbate neurodegeneration and cognitive deficits. This review explores the therapeutic potential of targeting metabolic pathways to mitigate AD pathology. Key metabolic disruptions, including insulin resistance, reduced cerebral glucose utilization, and mitochondrial inefficiency, are closely linked to neuronal energy deficits and synaptic dysfunction. Therapeutic approaches, such as insulin sensitizers, ketogenic diets, and mitochondrial-targeted antioxidants, have shown promise in preclinical and early clinical studies. Additionally, strategies to modulate lipid metabolism, such as enhancing cholesterol efflux via APOE or reducing neurotoxic ceramides, offer potential avenues for intervention. The review also highlights the roles of neuroinflammation and oxidative stress as mediators of metabolic dysfunction in AD, underscoring the need for multifaceted approaches that target both metabolic and inflammatory pathways. The emerging field of precision medicine offers opportunities to tailor interventions based on individual metabolic profiles, potentially enhancing treatment efficacy. Despite the growing recognition of metabolic dysfunction in AD, translating these insights into effective therapies remains challenging due to the disease's complexity and heterogeneity. Future research must focus on elucidating the interplay between metabolic pathways and AD pathology, identifying reliable biomarkers, and designing targeted interventions. By addressing the metabolic underpinnings of AD, this review underscores the potential of metabolic reprogramming as a novel and integrative therapeutic strategy to slow or prevent disease progression and improve patient outcomes.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Barnwal, N., Dubey, S., & Tiwari, P. K. (2025). Targeting Metabolic Dysregulation in Alzheimer’s Disease: A Potential Therapeutic Strategy. Current Drug Metabolism. https://doi.org/10.2174/0113892002408089250912080734
Vancouver
Barnwal N, Dubey S, Tiwari PK. Targeting Metabolic Dysregulation in Alzheimer’s Disease: A Potential Therapeutic Strategy. Current Drug Metabolism. 2025. doi:10.2174/0113892002408089250912080734. PMID: 40990282.
BibTeX
@article{barnwal2025-40990282,
author = {Barnwal, Nivedita and Dubey, Sonal and Tiwari, Prashant Kumar},
title = {{Targeting Metabolic Dysregulation in Alzheimer’s Disease: A Potential Therapeutic Strategy}},
journal = {Current Drug Metabolism},
year = {2025},
doi = {10.2174/0113892002408089250912080734},
pmid = {40990282},
url = {https://doi.org/10.2174/0113892002408089250912080734}
}
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Key findings
- Impaired glucose metabolism, mitochondrial dysfunction, oxidative stress, and lipid dysregulation are frequently observed in AD brains, suggesting that metabolic dysfunction may exacerbate neurodegeneration and cognitive deficits.
Why it matters
This review discusses metabolic problems such as impaired glucose metabolism, insulin resistance and mitochondrial dysfunction in Alzheimer's disease, and notes that insulin sensitizers, ketogenic diets and mitochondrial-targeted antioxidants have shown promise in preclinical and early clinical studies. It does not report a proven treatment or cure.
Study details
- Evidence strengthLow
How this study scored 33/100
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 (Current Drug Metabolism) |
| Journal's citation record | 1 / 4 | Current Drug Metabolism: journal h-index 139 (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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 2 / 7 | Cited 8 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 2.7 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 4.4× 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 8 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Prashant Kumar Tiwari: h-index 13 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Dayananda Sagar University: institution h-index 77 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40990282) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 33 / 100 | — |
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