Pharmacological Interventions in Vascular Dementia

Vascular dementia arises from cerebrovascular pathology, including small‐vessel disease, infarcts and chronic hypoperfusion, leading to progressive cognitive decline. Current pharmacological strategies seek to stabilise vascular integrity, protect the neurovascular unit and counteract secondary neurodegenerative processes. Established agents such as cholinesterase inhibitors and NMDA receptor antagonists offer modest symptomatic benefit by enhancing cholinergic transmission and modulating excitotoxicity. Emerging approaches target endothelial dysfunction, blood–brain barrier disruption, oxidative stress and neuroinflammation. Promising compounds include PPAR-γ agonists, antioxidant–anti-inflammatory conjugates and neurometabolic agents that restore mitochondrial function and energy homeostasis. Adjunctive use of antiplatelet or vessel‐protective therapies may slow progression of microvascular lesions. Despite these advances, no treatment yet halts disease progression, and future directions focus on multi-mechanistic regimens that integrate vascular stabilisation with neuroprotection and tissue repair. The global burden of vascular cognitive impairment underscores the need for accessible, cost-effective pharmacotherapies capable of addressing both vascular and neuronal targets.

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Pharmacological Interventions in Vascular Dementia publication trend

The graph below shows the total number of articles in pharmacological interventions in vascular dementia across all publications each year (not limited to Nature Index journals).

Technical terms

PPAR-γ receptor: Nuclear receptor that regulates genes involved in lipid metabolism, inflammation and vascular function.

Acetylcholinesterase: Enzyme responsible for breakdown of the neurotransmitter acetylcholine, a key target in dementia treatment.

Neurometabolic pharmacotherapy: Therapeutic approach aimed at supporting neuronal energy production and mitochondrial health in cerebrovascular disease.

Global cerebral ischaemia: Condition of widespread reduction in blood flow to the brain, causing diffuse neuronal injury and cognitive deficits.

Neurovascular unit: Functional complex of neurons, glial cells and blood vessels that maintains cerebral homeostasis and regulates blood flow.

References

1. Bergenin ameliorates cognitive deficits and neuropathological alterations in sodium azide-induced experimental dementia. Frontiers in Pharmacology (2022).
2. The Protective Effect of Dextran-Curcumin Conjugate on Memory Disorder in Animal Model of Global Cerebral Ischemia. Qom Univ Med Sci J (2018).
3. Neurometabolic pharmacotherapy in chronic cerebrovascular diseases. Meždunarodnyj Nevrologičeskij žurnal (2021).