Alzheimer’s Disease, Epilepsy, and Vascular Dementia: Convergent Mechanisms and Shared Therapeutic Pathways
Alzheimer’s disease (AD), epilepsy, and vascular dementia (VaD) are highly prevalent neurological diseases and lead global drivers of morbidity. While these conditions have been historically treated as distinct entities, they now appear to share convergent molecular and cellular processes that drive disease initiation and progression. This narrative review collates evidence from studies published from 2000 to 2025 to investigate overlapping mechanisms and therapeutic opportunities for the three conditions. Five interconnected mechanisms, excitotoxicity, neuroinflammation, oxidative stress, mitochondrial dysfunction, and vascular impairment, were identified as key driving processes resulting in self-sustaining cycles leading to neuronal injury, cognitive impairment, and seizure susceptibility. Clinically, this is represented by shared cognitive, behavioral, and functional impairments, and often, seizures can be overlooked during the dementia process. Therapeutic strategies which may be useful across diseases could include anti-inflammatory treatments, mitochondrial stabilizers, vascular health treatments, and protein aggregation changes. Important translational gaps also exist for practice particularly in the biomarker space and trials that allow intervention across diseases. Each of these conditions, in essence, represent the same inter-relationships at the level of pathophysiology and provides opportunities for multi-targeted treatment approaches and integrated research trajectories to ease the worldwide burden of neurodegenerative disorder.
Authors
- Md Ahsan Ghani (ORCID: https://orcid.org/0009-0001-2132-7999)
- Syed Haris Omar (ORCID: https://orcid.org/0000-0002-4955-5125)
Institutions
- Charles Sturt University (AU)
Publication Details
- Journal
- Journal of Vascular Diseases
- Published
- 2025-11-12
- DOI
- https://doi.org/10.3390/jvd4040044
- Primary Topic
- Alzheimer's disease research and treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00