Sporadic Alzheimer disease (AD) is a multifaceted neurodegenerative syndrome with complicated and unclear etiology that results in debilitating cognitive decline in old age. Although several decades of AD research resulted in major scientific advancements in identifying and tracking the disease, as well as discovering many salient genetic and environmental factors, considerably less progress in the development of efficacious therapies has been made. A major challenge for the field has been identifying sensitive and specific markers for detection in early stages of the disease, because by the time clinical symptoms are present, neuropathology is already quite advanced.1 Understanding the cascade of events that is unique to AD is complicated by the fact that AD exhibits a diverse clinical presentation and is often concomitant with other types of brain injury and dementia. A common example of this comorbidity is vascular disease, which can act as a risk factor for AD2 but also contributes to cognitive decline in its own right.3 Understanding the nature of the contributions of vascular pathology to AD is an important (and open) area of current research. Knowing if cerebrovascular disease plays an early and initiating role in the formation of AD neuropathology may have a significant impact on strategies to treat or even prevent the disease since vascular diseases are often highly responsive to treatment. However, cerebrovascular disease may simply occur in parallel to the development of AD pathology as a correlate and by-product of the aging process. Research examining the impact of various vascular health risk factors and specific neurovascular changes that can be measured in the human brain in vivo, along with biomarkers for AD (eg, β-amyloid [Aβ] positron emission tomography imaging of aggregated fibrillar amyloid plaque), are needed to elucidate this question.
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