Suspected non-AD pathology in mild cognitive impairment

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• 作者：Laura E.M. Wisse^a ; ^{Laura.Wisse@uphs.upenn.edu" class="auth_mail" title="E-mail the corresponding author} ; Nirali Butala^b ; Sandhitsu R. Das^a ; Christos Davatzikos^c ; Bradford C. Dickerson^d ; ^e ; Sanjeev N. Vaishnavi^b ; Paul A. Yushkevich^a ; David A. Wolk^b ; for the Alzheimer's Disease Neuroimaging Initiative¹
• 关键词：Suspected non-AD pathology ; Mild cognitive impairment ; Cerebrovascular disease ; Cognition ; Primary age-related tauopathy ; Amyloidosis
• 刊名：Neurobiology of Aging
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：36
• 期：12
• 页码：3152-3162
• 全文大小：741 K

文摘

We aim to better characterize mild cognitive impairment (MCI) patients with suspected non-Alzheimer's disease (AD) pathology (SNAP) based on their longitudinal outcome, cognition, biofluid, and neuroimaging profile. MCI participants (n = 361) from ADNI-GO/2 were designated “amyloid positive” with abnormal amyloid-beta 42 levels (AMY+) and “neurodegeneration positive” (NEU+) with abnormal hippocampal volume or hypometabolism using fluorodeoxyglucose–positron emission tomography. SNAP was compared with the other MCI groups and with AMY− controls. AMY−NEU+/SNAP, 16.6%, were older than the NEU− groups but not AMY− controls. They had a lower conversion rate to AD after 24 months than AMY+NEU+ MCI participants. SNAP-MCI participants had similar amyloid-beta 42 levels, florbetapir and tau levels, but larger white matter hyperintensity volumes than AMY− controls and AMY−NEU− MCI participants. SNAP participants performed worse on all memory domains and on other cognitive domains, than AMY−NEU− participants but less so than AMY+NEU+ participants. Subthreshold levels of cerebral amyloidosis are unlikely to play a role in SNAP-MCI, but pathologies involving the hippocampus and cerebrovascular disease may underlie the neurodegeneration and cognitive impairment in this group.