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.