Functional Neuroimaging of Memory Impairment
Speaker: Reisa Sperling , BWH, Harvard Medical School
Date: September 21 2006
Time: 2:00PM to 3:00PM
Location: 32-D507
Host: Polina Golland, CSAIL
Contact: Polina Golland, x38005, polina@csail.mit.edu
Relevant URL: Memory impairment is the clinical hallmark of mild cognitive
impairment (MCI) and Alzheimer's disease (AD), presumably due to
neuronal dysfunction in the hippocampal formation and functionally
connected regions of neocortex. Our fMRI studies have focused on the
neural substrates of associative memory processes, particularly
learning novel face-name associations, as difficulty remembering
proper names continues to be the most common complaint of older
individuals. We have demonstrated that patients with clinical AD have
decreased fMRI activation in the hippocampus and related structures
within the medial temporal lobe during the encoding of new memories,
compared to cognitively intact older subjects. More recently, fMRI
studies of subjects at risk for AD, by virtue of their genetics or
evidence of mild cognitive impairment (MCI), have yielded variable
results, suggesting there may be a phase of paradoxically increased
activation early in the course of prodromal AD. We hypothesize that
this hyperactivation may reflect compensatory processes to maintain
memory performance in the setting of early AD pathology, followed by
failure of hippocampal activation as memory impairment progresses.
Utilizing event-related fMRI techniques, which allow the separation of
MR signal associated with individual stimuli, based on whether the
face-name pair was subsequently remembered or forgotten, confirm that
activation in the anterior hippocampal formation is critical for
successful associative encoding in both young and older cognitively
intact subjects, and furthermore suggest that alterations in
neocortical cortical activity, particularly in medial parietal
regions, may underlie alterations in memory function in normal aging
and in early AD. We have incorporated multivariate analytic
techniques which provide new evidence that medial temporal lobe and
medial parietal neural activity are strongly correlated and that the
pathophysiologic process of AD disrupts a widely distributed memory
network. We are now combining fMRI with PET amyloid imaging techniques
to directly examine the impact of fibrillar amyloid deposition on
memory function.
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