Abstract
IntroductionAlthough widespread cortical asymmetries have been identified in Alzheimer's disease (AD), thalamic asymmetries and their relevance to clinical severity in AD remain unclear. MethodsLateralization indices were computed for individual thalamic subnuclei of 65 participants (33 healthy controls, 14 amyloid-positive patients with mild cognitive impairment, and 18 patients with AD dementia). We compared lateralization indices across diagnostic groups and correlated them with clinical measures. ResultsAlthough overall asymmetry of the thalamus did not differ between groups, greater leftward lateralization of atrophy in the ventral nuclei was demonstrated in AD, compared with controls and amyloid-positive mild cognitive impairment. Increased posterior ventrolateral and ventromedial nuclei asymmetry were associated with worse cognitive dysfunction, informant-reported neuropsychiatric symptoms, and functional ability. DiscussionLeftward ventral thalamic atrophy was associated with disease severity in AD. Our findings suggest the clinically relevant involvement of thalamic nuclei in the pathophysiology of AD.
Highlights
Widespread cortical asymmetries have been identified in Alzheimer's disease (AD), thalamic asymmetries and their relevance to clinical severity in Alzheimer’s disease (AD) remain unclear
Results: overall asymmetry of the thalamus did not differ between groups, greater leftward lateralization of atrophy in the ventral nuclei was demonstrated in AD, compared with controls and amyloid-positive mild cognitive impairment
We examined the degree of thalamic asymmetry in AD, spanning amyloid-positive mild cognitive impairment (MCI) and dementia
Summary
Widespread cortical asymmetries have been identified in Alzheimer's disease (AD), thalamic asymmetries and their relevance to clinical severity in AD remain unclear. The cerebral atrophy characteristic of AD is bilateral but may not be symmetrical across hemispheres. The degree of cerebral asymmetry in AD has been associated with poorer cognitive outcomes [6], greater disease severity [7], and neuropsychiatric symptoms [8,9]. The asymmetrical cerebral involvement in AD is considered to be nondirectional, or as Derflinger and colleagues describe it, “asymmetric but not lateralized” [4,5].
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