Abstract
BackgroundTo clarify whether atherosclerosis of the carotid and intracranial arteries is related to Alzheimer’s disease (AD) pathology in vivo, we investigated the associations of carotid and intracranial artery stenosis with cerebral beta-amyloid (Aβ) deposition and neurodegeneration in middle- and old-aged individuals. Given different variations of the pathologies between cognitive groups, we focused separately on cognitively normal (CN) and cognitively impaired (CI) groups.MethodsA total of 281 CN and 199 CI (mild cognitive impairment and AD dementia) subjects underwent comprehensive clinical assessment, [11C] Pittsburgh compound B-positron emission tomography, and magnetic resonance (MR) imaging including MR angiography. We evaluated extracranial carotid and intracranial arteries for the overall presence, severity (i.e., number and degree of narrowing), and location of stenosis.ResultsWe found no associations between carotid and intracranial artery stenosis and cerebral Aβ burden in either the CN or the CI group. In terms of neurodegeneration, exploratory univariable analyses showed associations between the presence and severity of stenosis and regional neurodegeneration biomarkers (i.e., reduced hippocampal volume [HV] and cortical thickness in the AD-signature regions) in both the CN and CI groups. In confirmatory multivariable analyses controlling for demographic covariates and diagnosis, the association between number of stenotic intracranial arteries ≥ 2 and reduced HV in the CI group remained significant.ConclusionsNeither carotid nor intracranial artery stenosis appears to be associated with brain Aβ burden, while intracranial artery stenosis is related to amyloid-independent neurodegeneration, particularly hippocampal atrophy.
Highlights
To clarify whether atherosclerosis of the carotid and intracranial arteries is related to Alzheimer’s disease (AD) pathology in vivo, we investigated the associations of carotid and intracranial artery stenosis with cerebral beta-amyloid (Aβ) deposition and neurodegeneration in middle- and old-aged individuals
For the Mild cognitive impairment (MCI) group, individuals 55–90 years old who fulfilled the core clinical criteria for diagnosis of MCI according to the recommendations of the National Institute on AgingAlzheimer’s Association (NIA-AA) guidelines [17] were included as follows: (a) memory complaints corroborated by the patient, an informant, or clinician; (b) objective memory impairment for age, education, and gender (i.e., at least 1.0 SD below the respective age, education, and gender-specific mean for at least one of the four episodic memory tests included in the Korean version of Consortium to Establish a Registry for Alzheimer’s Disease (CERAD-K) neuropsychological battery [Word List Memory, Word List Recall, Word List Recognition, and Constructional Recall test]); (c) largely intact functional activities; and (d) no dementia
Association of carotid and intracranial stenosis with AD biomarkers in the cognitively normal (CN) group In the exploratory step of the analyses, we found no significant differences in global Aβ deposition between CN subjects with vs. those without any type of stenosis (Table 3)
Summary
To clarify whether atherosclerosis of the carotid and intracranial arteries is related to Alzheimer’s disease (AD) pathology in vivo, we investigated the associations of carotid and intracranial artery stenosis with cerebral beta-amyloid (Aβ) deposition and neurodegeneration in middle- and old-aged individuals. Regarding in vivo brain imaging approaches, a couple of small-scale studies on individuals with severe cerebral hypoperfusion yielded inconsistent findings on the relationship between very severe atherosclerosis and beta-amyloid (Aβ) deposition [12, 13]. A recent study using high-resolution vessel wall magnetic resonance (MR) imaging reported that intracranial atherosclerotic plaque or stenosis was not associated with Aβ deposition in nondemented adults [14]. Knowledge of the association between carotid and intracranial atherosclerosis and other in vivo brain pathologies including regional neurodegeneration, as well as Aβ deposition, in the living human brain remains limited
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