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New York Consortium for Alzheimer Research and Education
The New York Consortium for Alzheimer Research and Education (N.Y.C.A.R.E.) is the joint effort of the Alzheimer’s Association New York City Chapter and the Education and Information Cores of the Alzheimer’s Centers — Columbia University, College of Physicians and Surgeons; Mount Sinai Medical Center; and New York University School of Medicine funded by the National Institute on Aging.

Early Detection Through Brain Imaging

The early identification of individuals at risk for Alzheimer’s disease (AD) is fundamental to developing preventative therapies. Recent years have brought a wealth of data indicating that it is possible to use brain imaging techniques to predict who is likely to experience cognitive decline and dementia.

A typical early feature of AD is that certain areas of the brain, called the medial temporal lobes, where the memory centers are located, shrink in volume, leading to impaired memory. The parietal lobe, which helps us orient our bodies in space and decipher where and what things are is also affected by Alzheimer’s disease. When Alzheimer’s begins destroying the parietal lobe, victims become lost and disoriented, even in familiar settings. They also begin mixing up objects, thinking that a computer is a television or that a mixing bowl is a soup pot. The frontal lobe, which also is affected, helps carry out purposeful behaviors and complex reasoning. When Alzheimer’s strikes the frontal lobe, the person loses the ability to plan and initiate complicated activities like balancing a checkbook.

These changes can be seen with standard brain imaging techniques like magnetic resonance imaging (MRI)
(Figure 1).

In addition to showing the structure of the brain, newer techniques are capable of monitoring changes in brain function. Different types of MRI can help examine how much blood is flowing through different areas of the brain (cerebral blood flow) or the concentrations of different substances in brain tissue. Changes in cerebral blood flow and chemical composition of the brain have been found in Alzheimer’s disease. Some researchers believe these changes can be detected before there are significant symptoms.

Positron emission tomography (PET) produces a three-dimensional image, and can show the metabolic rate of glucose by brain cells. It is known that healthy brain cells use more glucose than sick ones. PET scans show that patients with Alzheimer’s disease have reduced glucose uptake in the medial temporal lobes, parietotemporal, and frontal regions.

Similar, but less-severe reductions are also found in people who already show some memory impairment, but do not yet have AD. A scientist at one of the NYCARE partners, NYU Langone Medical Center, Center of Excellence on Brain Aging, has recently found evidence that there is a relationship between reduced glucose metabolism in AD-vulnerable brain regions and a maternal family history of AD in some cognitively normal individuals.

Although brain-tissue volume reductions, blood flow changes and decrease in glucose uptake are quite sensitive, they are not very specific to Alzheimer’s disease. They can also be seen in other diseases such as. stroke, epilepsy, and other types of dementia. They are not 100% predictive. This is an area that will require much additional study in the future.

Amyloid beta is a protein which accumulates in the brain during the progression of Alzheimer’s disease. It is so common that it is one of the hallmarks of this disease. An experimental PET scan study in which a compound called PIB is injected into the blood is able to reveal how much amyloid has been deposited, because PIB attaches itself to the amyloid and is visible with a PET scan. Multiple experimental compounds are being studied to determine whether they, too, will attach to brain amyloid deposits and can be detected by the PET scan. These new techniques will be a promising and significant supplement to magnetic resonance imaging and glucose uptake studies, and will undoubtedly contribute greatly to early detection of Alzheimer’s disease in the future.



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