Introduction     Diagnosis of Mild Cognitive Impairment and Alzheimer's Disease Karen L. Bell, M.D.     Treatment Strategies for Dementia and Mild Cognitive Impairment Mary Sano, Ph.D.     Treatment of Depression, Agitation, and Psychosis in Dementia Davangere P. Devanand, M.D.     Recognition of Vascular Dementia, Dementia with Lewy Bodies, and Frontotemporal Dementia Lawrence S. Honig, M.D., Ph.D.     Neuropsychology of Mild Cognitive Impairment, Alzheimer's Disease, Dementia with Lewy Bodies, and Frontotemporal Dementia Penne Sims, Ph.D.     Neuroimaging in Dementia Scott A. Small, M.D.     Neurobiological Correlates       Metabolism in Imaging       Imaging Modalities       Diagnostic Specificity       Early Detection       Genetics of Neurodegenerative Disease: Alzheimer's Disease, Frontotemporal Dementia Jennifer Williamson-Catania, M.S.     Legal and Ethical Issues for Patients with Dementia Daniel G. Fish, Esq.     Posttest         Accreditation     Reference List     Acknowledgements		Neuroimaging in Dementia Scott A. Small, M.D. Early Detection   We are on the cusp of offering effective treatment for Alzheimer's. Our treatments will be considered very effective if we can arrest progression of the disease upon detection; even the most optimistic neuropharmacologist is not expecting that we will reverse the disease process. We want to know whether can take any individual who presents with mild memory decline and test that person for hippocampal integrity. If a patient has hippocampal dysfunction we hope to be able to say, "Even though you are highly functioning and independent, you probably have early Alzheimer's disease."         Early Detection   The earliest deficit in Alzheimer's is a physiologic lesion in the hippocampus; as the disease progresses, it causes structural damage manifest as cell loss, plaques, and tangles in the brain. Courtesy of Dr. Scott Small     However, we know that there are multiple causes of hippocampal-dependent memory decline that come with aging. Early Alzheimer's is only one. How can we improve our diagnostic specificity to isolate early on the individuals who have Alzheimer's from those who have other causes of hippocampal dysfunction? The answer lies in the microanatomy of the hippocampus. There is reason to believe that different hippocampal subregions are targeted by different causes of age-related memory decline. Therefore we need very high spatial resolution for early detection.   In terms of disease pathogenesis, we know that Alzheimer's disease ultimately causes structural damage manifest as cell loss, plaques, and tangles. We now also know that the earliest deficit in Alzheimer's is not a structural lesion, it is a physiologic lesion. The cells might look normal under a microscope, so we need to use a technique that is sensitive to metabolism. Early detection requires a measure of metabolism and a microscopic resolution.   Alzheimer's is a slowly progressing disease, and imaging with a biomarker will tell us more quickly than a clinical trial whether a drug is effective. Imaging is thought to be more sensitive, and any of the modalities mentioned earlier might be helpful.   We still too often make a distinction between organic and functional disease. As Gowers said, "The term organic disease as commonly used means visible disease." Visibility is partly relative and it depends on the means of vision. I hope I have conveyed that the main impetus behind imaging is to enhance our ability to visualize disease as early as possible.     PREVIOUS | NEXT