ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Vasoactive neuropeptide dysregulation: A novel mechanism of microvascular dysfunction in vascular cognitive impairment.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Endogenous neuroprotection in vascular cognitive impairment and dementia.EBioMedicine · 2026Review
- From artery to memory: a comparative review of vascular cognitive impairment surgical models.Frontiers in aging neuroscience · 2026Review
- Vasoactive neuropeptide dysregulation: A novel mechanism of microvascular dysfunction in vascular cognitive impairment.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Non-Electrophilic Activation of NRF2 in Neurological Disorders: Therapeutic Promise of Non-Pharmacological Strategies.Antioxidants (Basel, Switzerland) · 2025Review
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10 authors.
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Abstract
introductionNeuropeptide dysregulation and microvascular injury are involved in pathogenesis of vascular cognitive impairment (VCI); however, the underlying etiology of this pathological axis remains unclear.
methodsWe investigated pathological mediators across varying severities of VCI in a rat model of chronic cerebral hypoperfusion (CCH). Proteomic analysis guided the evaluation of neuropeptide and non-neuropeptide markers associated with vascular and non-vascular dysfunction, which were correlated with cognitive function to determine their role in VCI.
resultsProteomic analysis revealed vasomotor dysfunction as the primary pathological pathway in VCI. Microvascular vasoconstriction was the earliest and most persistent event, initiating a cascade of both microvascular and non-vascular dysfunction. Dysregulation of vasoactive neuropeptides was identified as the key driver of this process. Calcitonin gene-related peptide (CGRP) supplementation effectively prevented vasoconstriction, and improved cognitive function in CCH. DISCUSSION: This study suggests dysregulation of vasoactive neuropeptides plays a central role in CCH pathomechanism, with microvascular vasoconstriction acting as the primary mediator. HIGHLIGHTS: Neuropeptides are the primary drivers of dominant pathomechanisms underlying chronic cerebral hypoperfusion (CCH). Early vasoactive neuropeptide dysregulation is a key driver of cognitive decline. Microvascular dysfunction precedes classical non-vascular pathologies in CCH. Capillary constriction precedes and drives amyloid accumulation in CCH. CGRP mitigates microvascular constriction, enhancing cognitive function in VCI.
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