Jeffrey Cummings, MD


May 29, 2012

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Hello. I am Jeffrey Cummings. I am the Camille and Larry Ruvo Chair for Brain Health at the Neurological Institute at Cleveland Clinic, and I am the Director of the Lou Ruvo Center for Brain Health in Las Vegas, Nevada. I would like to discuss some of the new material that emerged at the American Academy of Neurology meeting. One thing that caught my eye was a redefinition or a refinement of our idea of the sequence of events that evolves in the progression of Alzheimer's disease. We currently have a model in which amyloid beta changes first, followed by tau, followed by brain atrophy on MRI and FDG changes, and finally memory and functional changes.

New data presented this week by Dan Mungas[1] began to challenge and refine that model. Dan was able to show with his group that memory changes are occurring very early, essentially as early as the amyloid beta changes. So, it may not be that the cognitive impairment is delayed until substantial pathology is present, as reflected by MRI and tau, but rather the memory pathology is emerging very early in the disease and can be a measure of the progression of disease. We will be looking more carefully over time as we study this sequence of biomarkers in conjunction with the cognitive and functional abnormality of Alzheimer's disease.

Another abstract that I considered important came from the group of Bruno Dubois[2] in Paris. Bruno has been studying the hippocampal type of memory impairment that is characteristic of Alzheimer's disease and is identified with the Free and Cued Selective Reminding Test. He showed that when this type of memory abnormality of the hippocampal type is present, 90% of patients have abnormalities on biomarkers consistent with a diagnosis of Alzheimer's disease. They had either positive amyloid imaging or they had the cerebrospinal fluid signature of Alzheimer's disease, which is lowered amyloid beta, elevated tau, or both. It is important to note, however, that 10% of the patients who had the hippocampal type of abnormality did not have positive biomarkers for Alzheimer's disease, suggesting that both the hippocampal type of memory impairment and the biomarkers are going to be important for identifying those very early Alzheimer's disease patients.

Finally, I would like to talk about an abstract that I presented[3] that addressed the benefits of higher dose in the rivastigmine patch. We could see in earlier studies that patients who were treated with higher doses of rivastigmine were functioning at a better level. We confirmed that in the OPTIMA study using the 13.3-mg patch, and showed that if they were elevated to this dose from the 9.5-mg patch, then they did better functionally and cognitively. We think this is an important advance in terms of optimizing the treatment of Alzheimer's disease. Thank you.


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