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J Cereb Blood Flow Metab. 2015 Nov;35(11):1729-37. doi: 10.1038/jcbfm.2015.110. Epub 2015 Jun 3.

Hippocampal complex atrophy in poststroke and mild cognitive impairment.

Author information

1
Department of Neurology, Akershus University Hospital, Lørenskog, Norway.
2
Institute of Clinical Medicine, Campus Ahus, University of Oslo, Oslo, Norway.
3
Department of Artificial Intelligence, UNED, Madrid, Spain.
4
The Intervention Centre, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
5
Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
6
Department of Psychology, University of Oslo, Oslo, Norway.
7
Department of Geriatric Psychiatry, Akershus University Hospital, Lørenskog, Norway.
8
Department of Radiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
9
Department of Radiology, Akershus University Hospital, Lørenskog, Norway.

Abstract

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.

PMID:
26036934
PMCID:
PMC4635227
DOI:
10.1038/jcbfm.2015.110
[Indexed for MEDLINE]
Free PMC Article

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