Abstract: Dementia is a syndrome with various underlying pathologies acting independently or in concert to cause cognitive dysfunction. The development of disease-specific treatments and targeted prevention strategies requires precise clinical sub-typing via etiology and pathophysiological processes. Furthermore, recent research advances in biomarkers, especially for Alzheimer’s disease (AD) diagnosis, have improved diagnostic precision for dementia. This has led to the proposal of an AT(N) framework for AD diagnosis, with A, T, and N signifying the demonstrated presence of amyloid (A) and tau (T) pathologies as well as neurodegeneration (N) respectively. Many authors have proposed to add other pathophysiological mechanisms to the traditional AT(N) framework, such as neuroimmune dysregulation, synaptic dysfunction, and/or blood-brain barrier (BBB) alterations, to make the ATX(N) more accommodating of a range of pathologies important for dementia. This has included the special consideration of vascular pathogenesis being represented by a “V” (Sachdev, 2020). This indicates that cerebrovascular disease (CVD) is a common cause of dementia alone or in combination with AD, and the importance of developing biomarkers of vascular “V” brain pathology has been argued. Research progress in vascular cognitive impairment and dementia (VCID), the second most common cause of dementia, has however been slow, partly because of limited research in VCID relative to AD. The diagnosis of VCID presently relies mainly on clinical information and neuroimaging including magnetic resonance imaging and computed tomography. Consequently, there exists an imperative to develop molecular biomarkers for VCID with high sensitivity and accuracy.