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| |  Amyloid Beta-Peptide Levels Associated With Early Dementia CHICAGO, IL -- March 21, 2000 -- Levels of amyloid beta-peptide correlate with severity of dementia even early in the disease, according to an article in the March 22/29 issue of The Journal of the American Medical Association (JAMA). Jan Naslund, Ph.D., from Rockefeller University in New York, and colleagues analyzed brain tissue from the autopsies of 79 nursing home residents to determine levels of amyloid beta-peptide and tau protein. The patients studied had a range of dementia severity as measured by Clinical Dementia Rating (CDR) scores, which categorized patients as having: "no dementia" (CDR score of 0.0), or "questionable" (CDR score 0.5), "mild" (CDR score 1.0), "moderate" (CDR score 2.0) or "severe" (CDR score 4.0 or 5.0) dementia. The researchers analyzed the relationship of dementia severity with levels of two different lengths of amyloid beta-peptide (one with 40 amino acids, ABx-40, and another with 42 amino acids, ABx-42) in the brain tissue. They found elevated levels of both lengths of amyloid beta-peptide in patients classified as having questionable dementia to severe dementia. They also found that increases of both ABx-40 and ABx-42 were associated with increasing severity of dementia. Levels of ABx-42 were higher than ABx-40 in brain tissue of patients in all classifications, even those patients with no signs of dementia (CDR score of 0.0). One of the distinguishing features of Alzheimer disease, the most common type of dementia, is that brain tissue of patients with the disease has plaques that contain amyloid beta-peptide (a type of protein) and neurofibrillary tangles, which are composed of abnormal tau protein. Which of these components occur earliest in the disease has not be established because most autopsy studies evaluated patients with advanced dementia, when both plaques and tangles are present. Which occurs first is important because researchers could then focus efforts to treat or prevent Alzheimer disease on the brain pathology that occurs earliest in the disease. When the researchers analyzed the brain tissue for tau protein, they found that, at least in the frontal cortex region of the brain, amyloid beta-peptides appeared to precede the formation of neurofibrillary tangles with tau protein. "Our results suggest that levels of both ABx-40 and ABx-42 are elevated very early in the disease process, perhaps causing the onset of the pathological cascade that propagates the disease and ultimately leads to late-onset AD [Alzheimer disease]," the researchers write. "From a possible treatment perspective, attempts to prevent or slow the course of AD should focus on inhibiting the cellular production of [amyloid beta-peptides] and/or slowing the pathogenic assembly of [amyloid beta-peptides] into aggregates [deposits]." "Although causality of disease is not proven in a correlative study of the type presented here, the results argue in favor of a central role for [amyloid beta-peptide] early in the disease process," the researchers note. (JAMA. 2000;283:1571-1577) Related Link: The Journal of the American Medical Association (JAMA).
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