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Lisa Mosconi on Nutritional Medicine

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by Stacie Slotnick

Nov. 26, 2014

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Lisa Mosconi

Description

Alzheimer’s disease (AD) is the most common form of dementia, currently affecting over 5 million people in the USA alone. Age-related mild cognitive impairments may affect two to three times as many individuals. As pharmacological treatments for AD are limited, there has been growing interest in identifying non-pharmacological treatment strategies that focus on ameliorating individual medical and lifestyle risk factors as a way of delaying or preventing the onset of AD symptoms. Increasing evidence suggests that diet, a major modifiable lifestyle factor, may play a significant role in preventing or delaying cognitive decline and risk for dementia. While for many years, the general understanding was that AD was a disease of old age, recent breakthroughs in in vivo brain imaging techniques have reversed this paradigm by showing that the brain changes that lead to AD can be detected in predisposed individuals 20-30 years before clinical manifestations of disease become evident. The early appearance of pathological lesions and the progressive nature of cognitive deterioration in AD led to re-conceptualizing AD as a largely preventable illness. There is consensus that lifestyle interventions applied early in the course of AD may be more likely to achieve disease modification. Recent brain imaging studies have begun to clarify how diet and nutrition modulate AD risk in asymptomatic, cognitively normal individuals, especially those at increased genetic risk. There is evidence for associations between higher intake of dietary nutrients such as anti-oxidants, omega 3 polyunsaturated fatty acids, and B-complex vitamins, and reduced “brain AD-burden”, as reflected in reduced amyloid-beta (Aß) pathology (i.e., the major constituent of senile plaques) on Positron Emission Tomography (PET) with N-methyl[11C]2-(4'- methylaminophenyl)-6-hydroxy-benzothiazole (PiB); higher neuronal glucose metabolic rates on 2-[18F]fluoro-2-Deoxy-D-glucose (FDG)-PET, and larger brain volumes on Magnetic Resonance Imaging (MRI). This lecture will focus on the role of nature (genes) vs. nurture (lifestyle), and on biochemical individuality, as dementia-risk modulators, with an emphasis on brain imaging findings in the preclinical phase of AD. Such knowledge is critical prior to implementing lifestyle and dietary recommendations for prevention and treatment of disease.

This talk is part of the Advancing Wellbeing seminar series at the MIT Media Lab. For information about future talks, please join our mailing list by sending an email to wellness-seminars-join [at] media [dot] mit [dot] edu

Biography

Dr. Mosconi holds a PhD  in neuroscience and nuclear medicine from the University of Florence, Italy. She is an assistant professor of psychiatry at New York University (NYU) School of Medicine, the director of the Nutrition & Brain Fitness Lab at NYU, and a certified health coach and integrative nutritionist. Her National Institute of Health-funded research primarily focuses on the early detection of Alzheimer’s disease using biological markers such as positron emission tomography (PET) of glucose metabolism, amyloid deposition, neuro-receptor abnormalities and neuro-inflammation, and magnetic resonance imaging (MRI), and on the role of nature (i.e., genes) vs. nurture (i.e., environment, lifestyle) in modulating risk of age-related cognitive impairment and dementia. Dr. Mosconi is a member of the Society for Nuclear Medicine, the Alzheimer’s Association, the New York Academy of Sciences, and the Alzheimer’s Neuroimaging Workgroup of the Alzheimer’s Association. She has published over 100 peer-reviewed papers; has co-authored several book chapters, including Imaging the Aging Brain (Oxford University Press) and the New Encyclopedia of Neuroscience (Elsevier); and has served as guest editor for several peer-reviewed, international medical journals.

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