Hippocampal Complex Atrophy in Poststroke and Mild Cognitive Impairment

• Published in: Journal of cerebral blood flow and metabolism Vol. 35; no. 11; pp. 1729 - 1737
• Main Authors: Selnes, Per, Grambaite, Ramune, Rincon, Mariano, Bjørnerud, Atle, Gjerstad, Leif, Hessen, Erik, Auning, Eirik, Johansen, Krisztina, Almdahl, Ina S, Due-Tønnessen, Paulina, Vegge, Kjetil, Bjelke, Börje, Fladby, Tormod
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.11.2015; Sage Publications Ltd; Nature Publishing Group
• Subjects: Adult; Aged; Aged, 80 and over; Alzheimer Disease; Amyloid beta-Peptides - cerebrospinal fluid; Atrophy; Cerebrovascular Disorders - pathology; Cerebrovascular Disorders - psychology; Cognitive Dysfunction - pathology; Cognitive Dysfunction - psychology; Executive Function; Female; Hippocampus - pathology; Humans; Magnetic Resonance Imaging; Male; Memory; Mental Recall; Middle Aged; Neuropsychological Tests; Original; Psychomotor Performance; Reaction Time; Stroke - pathology; Stroke - psychology; tau Proteins - cerebrospinal fluid; White Matter - pathology; atherosclerosis; vascular cognitive impairment; white-matter disease; MRI; Alzheimer's
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.2015.110

To investigate putative interacting or distinct pathways for hippocampal complex substructure (HCS) atrophy and cognitive affection in early-stage Alzheimer's disease (AD) and cerebrovascular disease (CVD), we recruited healthy controls, patients with mild cognitive impairment (MCI) and poststroke patients. HCSs were segmented, and quantitative white-matter hyperintensity (WMH) load and cerebrospinal fluid (CSF) amyloid-β concentrations were determined. The WMH load was higher poststroke. All examined HCSs were smaller in amyloid-positive MCI than in controls, and the subicular regions were smaller poststroke. Memory was reduced in amyloid-positive MCI, and psychomotor speed and executive function were reduced in poststroke and amyloid-positive MCI. Size of several HCS correlated with WMH load poststroke and with CSF amyloid-β concentrations in MCI. In poststroke and amyloid-positive MCI, neuropsychological function correlated with WMH load and hippocampal volume. There are similar patterns of HCS atrophy in CVD and early-stage AD, but different HCS associations with WMH and CSF biomarkers. WMHs add to hippocampal atrophy and the archetypal AD deficit delayed recall. In line with mounting evidence of a mechanistic link between primary AD pathology and CVD, these additive effects suggest interacting pathologic processes.