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MEDIA CONTACT: Elizabeth
Crown at (312) 503-8928 or at e-crown@northwestern.edu
May 27, 2003
Brain Tangles Occur in Normal Aging
CHICAGO --- Accumulation of neurofibrillary tau tangles not only
causes the memory loss that occurs in Alzheimer’s disease but
also may be responsible for the memory deficits seen in normal aging
and in some cases of mild cognitive impairment, a study from Northwestern
University and the University of Miami has found.
Mild cognitive impairment is isolated memory loss more severe than what is associated
with “normal aging,” but without the additional cognitive difficulties
or disruptions of daily living activities characteristic of Alzheimer’s
disease.
Individuals with mild cognitive impairment have been shown to develop Alzheimer’s
at a higher rate than those without cognitive impairment, suggesting that mild
cognitive impairment may represent an intermediate stage between aging-related
memory loss and Alzheimer’s disease.
Angela L. Guillozet, a researcher in the Cognitive Neurology and Alzheimer’s
Disease Center at Northwestern University, and colleagues reported in the May
issue of Archives of Neurology that neurofibrillary tangles are more numerous
in brain regions associated with memory function and correlate with performance
on memory tests in cognitively normal elderly persons and those with mild cognitive
impairment.
The group’s study also showed that beta-amyloid plaques, the other diagnostic
marker for Alzheimer disease -- which some researchers believe cause the memory-robbing
neurodegeneration that occurs in Alzheimer’s -- do not play a significant
role in cognitive status prior to the development of Alzheimer’s disease.
The researchers investigated tangle distribution in the brain and neuropsychological
test results in five persons with no cognitive impairment and three with mild
cognitive impairment who had agreed to donate their brain after death. The last
test occurred between 15 days and a little over a year before death.
They found that individuals with mild cognitive impairment had higher densities
of neurofibrillary tangles than did nonimpaired persons. In addition, tangle
density in brain regions associated with memory function correlated with scores
on memory tests, but density of beta-amyloid did not.
Results of their study indicate that neurofibrillary tangles may constitute the
basis of memory loss not only in Alzheimer’s disease but also in normal
aging and mild cognitive impairment. Further, the results seem to confirm findings
from other studies that discerned no relationship between amyloid distribution
and dementia severity in Alzheimer’s disease.
Guillozet is postdoctoral student at the Feinberg School of Medicine at Northwestern
University. Her co-researchers at the Feinberg School were Sandra Weintraub,
professor of psychiatry and behavioral sciences and M.-Marsel Mesulam, M.D.,
Ruth and Evelyn Dunbar Professor of Psychiatry and Behavioral Sciences, professor
of neurology and director of the Cognitive Neurology and Alzheimer’s Disease
Center. Deborah C. Mash of the University of Miami School of Medicine also contributed
to the study.
This study was supported by grants from the National Institute on Aging and from
the National Institute of Neurological Disorders and Stroke, National Institutes
of Health.
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