Hippocampal complex atrophy in poststroke and mild cognitive impairment

Area of Science:

• Neuroscience
• Neurology
• Radiology

Background:

• Investigating the distinct or interacting pathways of hippocampal complex substructure (HCS) atrophy and cognitive impairment in early Alzheimer's disease (AD) and cerebrovascular disease (CVD).
• Understanding the relationship between white-matter hyperintensity (WMH) load, cerebrospinal fluid (CSF) amyloid-β concentrations, and HCS atrophy in healthy controls, mild cognitive impairment (MCI), and poststroke patients.

Purpose of the Study:

• To differentiate and identify interacting pathways leading to HCS atrophy and cognitive deficits in early AD and CVD.
• To examine the association between WMH load, CSF amyloid-β levels, and HCS volume in different patient groups.

Main Methods:

• Recruitment of healthy controls, patients with MCI, and poststroke patients.
• Segmentation of HCSs, quantitative assessment of WMH load, and measurement of CSF amyloid-β concentrations.
• Correlation analysis between HCS size, WMH load, CSF amyloid-β levels, and neuropsychological test results.

Main Results:

• Higher WMH load observed in poststroke patients.
• Amyloid-positive MCI patients showed smaller HCSs and reduced memory, while poststroke and amyloid-positive MCI patients exhibited reduced psychomotor speed and executive function.
• HCS size correlated with WMH load in poststroke patients and CSF amyloid-β in MCI patients. Neuropsychological function correlated with WMH load and hippocampal volume in both poststroke and amyloid-positive MCI groups.

Conclusions:

• CVD and early AD exhibit similar HCS atrophy patterns, but differ in their associations with WMH and CSF biomarkers.
• WMHs exacerbate hippocampal atrophy and memory deficits (delayed recall) in AD, indicating additive pathological processes.
• The findings suggest interacting pathological mechanisms between AD and CVD, contributing to cognitive decline.