Potential of PET/CT in assessing dementias with emphasis on cerebrovascular disorders
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EDITORIAL
Potential of PET/CT in assessing dementias with emphasis on cerebrovascular disorders Austin J. Borja 1,2 & Emily C. Hancin 1,3 & Vincent Zhang 1 & Mona-Elisabeth Revheim 1,4,5 & Abass Alavi 1
# Springer-Verlag GmbH Germany, part of Springer Nature 2020
Vascular dementia is a progressive cerebrovascular disorder caused by reduced blood flow to the brain, which may lead to significant loss of brain function [1]. This cerebrovascular disease has an estimated prevalence of 1–4% of adults over age 65, a percentage that approximately doubles every 10 years [2]. The progression of vascular dementia depends on numerous factors, including age-related risks such as hypertension, diabetes, and hyperlipidemia, which lead to the buildup of atherosclerotic plaques in the carotid arteries [3, 4]. Moreover, many cases of dementia have been reported to display both Alzheimer’s disease (AD) and vascular dementia traits, and over 80% of AD cadavers show evidence of cerebrovascular disease [5]. A molecular imaging approach using positron emission tomography (PET) for the detection and diagnosis of atherosclerosis upstream of vascular dementia could have a substantial impact on treating an aging population suffering from cognitive impairment. It is well-established that the brain has high metabolic demands, primarily to maintain neuronal membrane potential and ionic homeostasis. Although the brain constitutes just 2% of adult body mass, up to 20% of cardiac output is directed toward cerebral blood flow [6]. Moreover, prolonged disruption of either oxygen or glucose supply to the brain may result in irreversible neuronal cell damage in a matter of minutes [7]. Consequently, hypoxia secondary to vascular disease can lead
to profound impact on cognitive function [8–11]. Prolonged cerebrovascular disease for years is considered a major cause of age-related cognitive decline [12–14]. Vascular dementia, a progressive cerebrovascular disease, is caused by reduced cerebral blood flow and possible emboli and eventually leads to significant loss of brain metabolism and function [15–17]. Individuals at the highest risk for vascular dementia are those with a recent history of stroke or transient ischemic attacks [18, 19]. While these episodes would lead to an acute decline in cognitive function, prolonged alterations in cerebral blood flow over years or decades will also result in profound loss of cognitive function [20]. Preliminary data from our lab has showed that subjects with cardiovascular risk factors demonstrate significantly lower FDG uptake values compared with age- and sex-matched healthy controls (Fig. 1). These findings suggest an association between cardiovascular risk factors and altered global brain metabolism. The development of vascular dementia is far from uniform. In many cases, vascular dementia is stroke-related, following either a large stroke or a series of smaller strokes [21]. This form of vascular dementia leads to long periods of normalcy, interjected with short time points of sudden decline of cognitive
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