Neuroscience 2001 Abstract
Presentation Number: | 463.3 |
---|---|
Abstract Title: | <i>IN VIVO</i> DETECTION OF NEUROPATHOLOGY IN AN ANIMAL MODEL OF ALZHEIMER'S DISEASE BY MAGNETIC RESONANCE IMAGING. |
Authors: |
Helpern, J. A.*1
; Wisniewski, T.1
; Duff, K.1
; Dyakin, V.1
; de Leon, M.1
; Ardekani, B.1
; Wolf, O.1
; Branch, C.1
; O'Shea, J.1
; Wegiel, J.2
; Nixon, R. A.1
1Nathan Kline Institute/New York University School of Medicine, Orangeburg, NY 2Institute for Basic Research, Staten Island, NY |
Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neurodegenerative Disorders -- Alzheimers Disease: Other |
Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Genetic Models |
Session: |
463. Neurodegenerative disorders: Alzheimer's disease--pathology and imaging Slide |
Presentation Time: | Tuesday, November 13, 2001 8:30 AM-8:45 AM |
Location: | Room 30C |
Keywords: | NEURODEGENERATION, BETA AMYLOID, PRESENILIN, AMYLOID PRECURSOR PROTEIN |
The cerebral deposition of amyloid β-peptide, a central event in Alzheimer's disease (AD) pathogenesis, begins several years before the onset of clinical symptoms. Non-invasive detection of AD pathology at this initial stage would facilitate intervention and enhance treatment success. Here, we demonstrate the ability of high field strength MRI to detect regional brain volume reductions and ventricular enlargement in the PS-APP transgenic mouse model of AD more sensitively than histopathologic analysis by unbiased stereology. Moreover, the transverse relaxation time T2, an intrinsic MR parameter thought to reflect impaired cell physiology, was altered substantially in cortical regions containing β-amyloid but only slightly in cerebellum, which contains little β-amyloid. MR measures were also minimally altered in mice expressing mutant presenilin-1, which do not deposit β-amyloid, supporting the view that the MR abnormalities in PS-APP mice are partly related to amyloid β-peptide deposition. These results set the stage for MRI to aid in the early diagnosis of AD and the evaluation of potential therapies in transgenic animal models and in patients.
Supported by NIA(AG17617)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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