Alzheimer’s Disease Associated with Beta Protein Buildup

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Researchers have long suspected that the buildup of plaques made of clumps of amyloid-beta protein associated with cognitive deterioration and Alzheimer’s disease. These deposits are apparently toxic protein peptide that settles between the brain’s nerve cells, according to the National Institutes of Health National Institute on Aging. The deposit buildup can be accelerated by clogged arteries, high blood pressure, diabetes, concussion and inflammation.

While current treatments can ease the symptoms, they don’t slow the disease. Alzheimer’s disease affects more than 5.4 million American’s and is considered the costliest disease surpassing heart and cancer disease. Approximately, 4.1 million patients require intensive care amounting $200 billion every year.  Alzheimer’s patients live an average of four to eight years after the diagnosis but could live as long as 20 years, with 75 percent of them going to nursing home by age 80.

The game changer came last year with the FDA approval of Amyvid, an amyloid imaging agent to help researchers track the plaque in PET scans. They found that plaque removal doesn’t help patients in advance stages where the plaque has already done irreversible damage. Scientists and researchers are doing clinical trials to remove the plaque from patients in the early stage of the disease.

According to a new study, it may not be the plaque buildup but the brain location where the clump of abnormal proteins are developed. Scientists and researchers believe that they can predict the overall risk of the disease by tracing the sites of plaque buildup.

Amyloid plaque begins to accumulate early in the temporal lobe which is associated with the cognitive decline in contrast to other areas, according to the study of investigators from Penn Medicine’s Department of Radiology and published in Neurobiology of Aging journal.

Discerning the probability of Alzheimer’s disease is a high priority for health policy experts and health care professionals as the population about 65 could increase by 74 percent in 2020.

Current assessment methods used to determine the memory decline and Alzheimer’s are amyloid plaque neuroimaging, and physical and fluid tests. While previous studies in dementia-free people are associated with greater amounts of plaque and higher risk of developing the disease, it has been found recently that cognitive deterioration is not evident in one-third of individuals with plaque in their brain.

In collaboration with a team led by Susan M. Resnick, Ph.D., at the National Institute on Aging (NIA), Davatzikos and his Penn colleagues discovered that it’s the amyloid plaque spatial pattern progression rather than the total amount of plaque found in the brain.

A study analyzing the PET PiB scans of 64, 76 years-old patients, conducted by first author Rachel A. Yotter, Ph.D., a postdoctoral researcher in the Section for Biomedical Image Analysis and her team from the NIA’s Baltimore Longitudinal Study of Aging created unique image of their brain and analyzed the PET images to identify and determine amyloid temporal modification.

Notwithstanding the disparity in the combined amount of amyloid in the brain of most stable and most declining participants, the spatial sequences between the two groups were variant, with the former showing proportionately early accumulation in the frontal lobes and the latter in the temporal lobes.

Their finding gave them broad understanding of the link between resistance and cognitive deterioration with amyloid plaque trajectory affecting the brain early or later in disease progression.

Researchers are still investigating more patients with mild cognitive impairment that may shed light on the relevance of early detection associated with a clump of amyloid beta protein plaque buildup in Alzheimer’s disease.

Written by: Janet Grace Ortigas

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