Annals of the New York Academy of Sciences
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Ann. N. Y. Acad. Sci. · Apr 2000
Traumatic brain injury elevates the Alzheimer's amyloid peptide A beta 42 in human CSF. A possible role for nerve cell injury.
The increased risk for Alzheimer's Disease (AD) associated with traumatic brain injury (TBI) suggests that environmental insults may influence the development of this age-related dementia. Recently, we have shown that the levels of the beta-amyloid peptide (A beta 1-42) increase in the cerebrospinal fluid (CSF) of patients after severe brain injury and remain elevated for some time after the initial event. The relationships of elevated A beta with markers of blood-brain barrier (BBB) disruption, inflammation, and nerve cell or axonal injury were evaluated in CSF samples taken daily from TBI patients. ⋯ Similar or better correlations were observed between A beta 1-40 and the three aforementioned markers. These results imply that the degree of brain injury may play a decisive role in determining the levels of A beta 1-42 and A beta 1-40 in the CSF of TBI patients. Inflammation and alterations in BBB may play lesser, but nonetheless significant, roles in determining the A beta level in CSF after brain injury.
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Most necropsy surveys of dementia have found that vascular disease is second only to Alzheimer's disease as a cause of dementia. Alzheimer's disease and cerebrovascular disease also often coexist. The purpose of the present study was to determine the nature of the cerebrovascular lesions that are most significant in producing dementia. ⋯ Severe cribriform change and deep white/grey matter micro-infarcts were significantly more common in the test group than in either of the control groups, whereas single macroscopic infarcts were more common in the stroke control group than either of the other two groups. Thus, microvascular deep white and grey matter lesions, but not macroscopic infarction, were significant in vascular dementia. The results of this study will be discussed in relation to the view that microvascular lesions may also contribute to dementia in subjects with more extensive Alzheimer-type pathology and thus lower the threshold at which Alzheimer-type pathology becomes clinically manifest.