Monthly Archives: February 2019

Amyloid PET Identifies Those At Risk For Alzheimer’s Disease

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Michael Mega, MD, PhD Director, Center for Cognitive Health

        The definition of Alzheimer’s disease is changing. With the ability to visualize beta amyloid, the predominate protein that makes up the plaques in Alzheimer patient’s brains, physicians now can tell who is at risk for the disease. Prior to the advent of amyloid PET scans, and spinal fluid analysis of beta amyloid, the certain diagnosis of Alzheimer’s disease was only made at death by microscopic evaluation of amyloid plaque burden. Now with the ability to visualize amyloid burden in life we have a window on how the disease evolves.

Alzheimer’s disease was once defined as a clinical presentation of a memory disorder with a decline in another domain of thinking (either language, visual-spatial processing, or problem solving) that is severe enough to interfere with daily functioning. Although many brain diseases can interfere with daily functioning to cause “dementia,” Alzheimer’s disease is the number one cause of dementia. Using this old definition of Alzheimer’s disease, investigators found that 15-20% of patients had o amyloid deposited in their brains on Amyloid PET scans. These patients may have diluted the findings in clinical trials testing amyloid lowering agents that hoped to slow or stop the disease. For this reason the definition of Alzheimer’s disease has moved from the old clinical description to a biological diagnosis. Now a person can only have Alzheimer’s disease when they are found to have an abnormally high amount of amyloid in their brain.

We all produce beta amyloid in our brains. Those of us who develop Alzheimer’s disease either make too much amyloid or do not clear it properly. Amyloid PET scans have shown the beginnings of amyloid accumulation in people as young as 30 to 40 years old. When a cognitively normal person has an abnormally high amount of amyloid in their brain they are now said to have preclinical Alzheimer’s disease; if they have a slight memory problem they meet the definition of prodromal Alzheimer’s disease, when their memory and thinking dysfunction is severe enough to interfere with daily life they are said to have full-blown Alzheimer’s dementia.

Selective amyloid lowering agents appear not to work in full-blown Alzheimer’s dementia. Can these new drugs work in the earlier stages of the disease in people with positive Amyloid PET scans? That is a question that our aging society is waiting to answer.  

Photo Caption:

Amyloid PET scans show amyloid deposits in red in the brains of people with Alzheimer’s disease. A&B) Patients scanned at screening and after 78 weeks of treatment with the selective amyloid lowering agent: bapineuzumab, note the reduction in amyloid deposition. C&D) Patients given placebo in the same study, note increased accumulation of amyloid in their brains.

How to Lower Your Risk for Alzheimer’s Disease

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Michael Mega, MD, PhD Director, Center for Cognitive Health

Do you have a family history of Alzheimer’s disease? If you do there is much you can do now to reduce the chances of developing the disease even if you are carrying genes that increase your risk. Your lifestyle can turn on genes that fight disease and turn off those that increase the risk for disease. We are just beginning to understand that the foods we eat, our physical activity, how we deal with stress, and the cognitive stimulation we receive from our work or pastimes can influence our risk for developing Alzheimer’s disease.

Reducing many of the risks for cardiovascular disease also reduce the risk for Alzheimer’s disease. The food we eat can be medicine, or poison. The most harmful “food” we consume is refined sugar. The higher our daily dose of this manmade poison the greater our risk for developing obesity, diabetes, stroke, heart attack, and Alzheimer’s disease. Embracing a Mediterranean diet low in simple carbohydrates and high in fruits, vegetables, nuts, olive oil, and seafood is associated with a reduction of Beta-amyloid, the protein thought to cause Alzheimer’s disease (see figure below.)

Increasing our physical activity with aerobic exercise by as little as 20 minutes every other day has been associated with improvements in cognitive testing in patients with Mild Cognitive Impairment (MCI), a condition thought to be prodromal Alzheimer’s disease when Beta-amyloid is abnormally high in the brain. Stress, or administration of the stress hormone glucocorticoid, increases Beta-amyloid and the protein that makes up the microscopic tangles in the brain involved in synaptic dysfunction and neuronal death associated with Alzheimer’s disease. Thus, stress reduction through mindfulness, biofeedback, and yoga can reduce disease risk.

Learning new information increases the density of the connections, or synapses, between brain cells; these synapses are pruned early in the disease. Increased synaptic density, occurring through cognitive stimulation increases our cognitive reserve. The higher our cognitive reserve the lower our risk for developing Alzheimer’s disease. So if you don’t use it you will loose it. Now is the time to modify your lifestyle to prevent Alzheimer’s even if you have a history of the disease.

Photo Caption:  Amyloid PET scans showing two-year increase in amyloid deposits in the brains of 36 cognitively healthy people who did not adhere to a Mediterranean diet compared to 34 who did adhere to the diet. These data support a 1.5-3.5 year protection against Alzheimer’s disease when people follow a Mediterranean diet for only 2-3 years. (Berti, V et al. Neurol 2018; 90:e1798)