Publication:

Hippocampal Hyperperfusion in Alzheimer's Disease

Loading...
Thumbnail Image

Date

2008-10-01

Journal Title

Journal ISSN

Volume Title

Publisher

Elsevier BV
The Harvard community has made this article openly available. Please share how this access benefits you.

Research Projects

Organizational Units

Journal Issue

Citation

Alsop, David, Melynda Casement, Cedric de Bazelaire, Tamara Fong, Daniel Press. "Hippocampal Hyperperfusion in Alzheimer's Disease." NeuroImage 42, no. 4 (2008): 1267-1274. DOI: 10.1016/j.neuroimage.2008.06.006

Abstract

Many of the regions with the earliest atrophy in Alzheimer’s Disease (AD) do not show prominent deficits on functional imaging studies of flow or metabolism. This paradox may provide unique insights into the pathophysiology of AD. We sought to examine the relationship between function and atrophy in AD using MRI blood flow and anatomic imaging. 22 subjects diagnosed with AD, mean Mini Mental State Exam (MMSE) score 22.2, and 16 healthy elderly controls were imaged with a volumetric arterial spin labeling blood flow MRI technique and an anatomical imaging method using the identical spatial resolution, image orientation, and spatial encoding strategy. Cerebral blood flow(CBF) and gray matter (GM) maps derived from the imaging were transformed to a standard anatomical space. GM and CBF maps were tested for significant differences between groups. Additionally, images were tested for regions with significant mismatch of the CBF and GM differences between groups. CBF was significantly lower in the bilateral precuneus, parietal association cortex and the left inferior temporal lobe but was non-significantly increased in the hippocampus and other medial temporal structures. After correction for GM loss, CBF was significantly elevated in the hippocampus and other medial temporal structures. The hippocampus and other regions affected early in AD are characterized by elevated atrophy-corrected perfusion per cc of tissue. This suggests compensatory or pathological elevation of neural activity, inflammation, or elevated production of vasodilators.

Description

Research Data

Keywords

Cognitive Neuroscience, Neurology

Terms of Use

This article is made available under the terms and conditions applicable to Other Posted Material (LAA), as set forth at Terms of Service

Endorsement

Review

Supplemented By

Related Stories