Semin Neurol 2013; 33(04): 313-329
DOI: 10.1055/s-0033-1359319
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Alzheimer's Disease

Carly Oboudiyat
1  Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida
,
Hilary Glazer
1  Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida
,
Alon Seifan
2  Department of Neurology, Columbia University College of Physicians and Surgeons, New York, New York
,
Christine Greer
1  Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida
,
Richard S. Isaacson
3  Department of Neurology, Weill Cornell Medical College, New York, New York
› Author Affiliations
Further Information

Publication History

Publication Date:
14 November 2013 (online)

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative cause of dementia and is responsible for significant individual morbidity and mortality, and economic impact on the health care system. Neurodegeneration (including neuronal atrophy and/or loss) are attributed to extraneuronal toxic amyloid oligomers and proteins, intraneuronal neurofibrillary tangles consisting of hyperphosphorylated tau, region-specific diminished cerebral glucose metabolism, synaptic dysfunction, and mitochondrial dysfunction. Several of these pathologic changes may occur decades before symptom onset, leaving ample time for implementing prevention strategies that target the earliest stages of the disease. In recent years, a myriad of modifiable and nonmodifiable risk factors have been elucidated. We describe the latest criteria for the diagnosis of AD, including earliest diagnostic stage of preclinical AD, which has the highest potential for research, including diagnosis and disease modification. We discuss both FDA-approved pharmacologic treatments, as well as nonpharmacologic strategies for AD therapeutics, including prevention via evidence-based, low-risk interventions. Genotype is an important consideration in managing patients on the AD continuum, as presence of the APOE ε4 allele may influence response to treatment. We present the most current evidence relating to pharmacogenomics, nutrigenomics, and distinctive nutritional requirements targeted toward AD.