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First Comprehensive Amyloid Imaging Solution1

When evaluating for Alzheimer’s disease and other causes of cognitive decline

Patients with symptoms of cognitive impairment can be misdiagnosed with Alzheimer's disease. In fact, up to one in five patients clinically diagnosed with probable Alzheimer’s disease during life do not have Alzheimer’s disease pathology upon autopsy.7,8

Illustration of brain with Alzheimer's disease
Illustration of brain with Alzheimer's disease

 

Only neuropathological examination, usually performed at autopsy, can definitively rule out Alzheimer’s disease.3 For the first time in clinical practice, physicians can now utilize PET/CT imaging to estimate beta-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's disease and other causes of cognitive decline.

 

Beta-amyloid plaque is one of the necessary pathological features of Alzheimer’s disease. Beta-amyloid plaques are deposits of a protein fragment called beta-amyloid that build up in the spaces between nerve cells (neurons) in the brain. In a healthy brain, beta-amyloid protein fragments are broken down and removed from the brain. In a brain with Alzheimer’s disease, beta-amyloid protein fragments accumulate to form hard, insoluble plaques in between neurons. Beta-amyloid accumulation builds over many years in the brain.9 Accumulation of beta-amyloid plaques interacts with a signal pathway that causes neurofibrillary tangles which are insoluble twisted fibers found inside the brain’s cells. As increasing amounts of plaques and tangles form in particular areas of the brain, brain cells work less efficiently, eventually losing their ability to function and, ultimately, dying. As beta-amyloid plaques are seen in other neurologic conditions and older people with normal cognition, confirmation of beta-amyloid plaques does not definitively lead to Alzheimer’s disease diagnosis. It is, therefore, important to have access to innovative technologies that can help differentiate and quantify amyloid-plaque buildup in the living brain.
 

 

3 Hyman BT, Phelps CH, Beach TG, et al. National Institute on Aging–Alzheimer’s Association Guidelines for the Neuropathologic Assessment of Alzheimer’s Disease. Alzheimers Dement. 2012;8:1-13.
7 Lim A, Tsuang D, Kukull W, et al. Clinico-Neuropathological Correlation of Alzheimer’s Disease in a Community-Based Case Series. J Am Geriatr Soc. 1999;47(5):564–569.
8 Petrovitch H, White LR, Ross GW, et al. Accuracy of Clinical Criteria for AD in the Honolulu-Asia Aging Study, a Population-Based Study. Neurology. 2001;57(2):226–234.
9 Rodriguez KM, Kennedy KM, Devous MD Sr, et al. Amyloid Burden in Healthy Aging: Regional Distribution and Cognitive Consequences. Neurology. 2012;78(6):387-95.

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