Levels of Protein Aβ42 in the Spinal Fluid, Detects Presence of Early Stage of Alzheimer's Disease
Filed in archive Diagnostics , Studies on July 24, 2006
According to a report in the July issue of the Archives of Neurology (one of the JAM/Archives Journal), early signs of the development of Alzheimer's disease can be detected in the cerebrospinal fluid of middle-aged adults who are genetically predisposed to the neurologic condition.
According to background information in the article, there are two strongest risk factors of having Alzheimer's disease: aging and the presence of an allele (type of gene) known as apolipoprotein E 4 (APOE 4).
The following are already known about Alzheimer's disease:
1) APOE 4 allele carriers develop clinical dementia about 10 to 15 years earlier than those who do not have it.
2) The plaque in the brain (causing Alzheimer's) made of proteins known as β-amyloids, begin forming years before affected individuals experience any symptoms of the disease.
3) As these β-amyloid proteins (predominately type Aβ42) clump together, fewer are available to circulate through the nervous system.
Thus, lower levels of the Aβ42 in the cerebrospinal fluid surrounding the brain and spinal cord serve as biomarkers or chemical indicators of the development of Alzheimer's disease.
The research team from VA Puget Sound Health Care System and University of Washington School of Medicine (Seattle) estimated the combined effect of aging and the APOE 4 allele on levels of Aβ42 and another β-amyloid (Aβ40) in 184 adults.
"These findings have implications for the preclinical diagnosis of Alzheimer's disease, as well as for treatment," the authors conclude.
"Therapeutic strategies aimed at prevention of Alzheimer's disease may need to be applied in early midlife or even younger ages to have maximal effect on amyloid deposition.
Primary prevention trials for Alzheimer's disease targeting elderly persons may be too late to affect the early stages of disease pathology."
Read more at Science Daily.

"Therapeutic strategies aimed at prevention of Alzheimer's disease may need to be applied in early midlife or even younger ages to have maximal effect on amyloid deposition.
Primary prevention trials for Alzheimer's disease targeting elderly persons may be too late to affect the early stages of disease pathology."
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