Collaborate 2 Cure
May 1, 2017

 

Location

KU Clinical Research: Fairway Auditorium
4350 Shawnee Mission Parkway Fairway, KS 66205

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Mitochondria in Alzheimer’s Disease

Abstract

What initiates Alzheimer’s disease (AD) histology changes in those with late-onset AD (LOAD) is unclear. An association between advancing age, AD histology changes, and AD incidence suggests brain aging-related factors may play a role or even initiate the disease. Brain energy metabolism and mitochondrial function change with advancing age and in AD, leading some to propose a “mitochondrial cascade hypothesis” in which bioenergetic changes are hypothesized to initiate AD histology and clinical decline. This presentation reviews brain aging and AD-associated changes in brain energy metabolism, considers whether these changes may play a relatively upstream and important role in LOAD, and discusses whether targeting brain energy metabolism offers a reasonable and practical therapeutic strategy. 

Speaker- Russell Swerdlow, MD

Dr. Russell Swerdlow is a physician-scientist at the University of Kansas.  He directs the NIH-funded University of Kansas Alzheimer’s Disease Center, serves as an attending physician at the Kansas University Medical Center’s Memory Disorders Clinic, directs the Kansas University Medical Center’s Neurodegenerative Disorders Program, and is a professor in the Departments of Neurology, Molecular and Integrative Physiology, and Biochemistry and Molecular Biology at the University of Kansas School of Medicine. 

 

Association of Inherited Mitochondrial Genomic Variants with Alzheimer’s Disease

Abstract

Evidence from a variety of studies suggest inherited mitochondrial DNA (mtDNA) variation influences Alzheimer’s disease (AD) risk.  However, reports of mtDNA variations are not consistent thus weakening the claim of linkages between inherited mtDNA variations and AD.  To address this we deep sequenced mtDNA from 85 AD and 170 control subjects and found 22 single nucleotide variants (SNVs) and one deletion that occurred at a significantly higher frequency in either the AD or control subjects.  The majority of these SNVs, 14 plus the one deletion, occurred more frequently in the AD group.  Among the 14 AD-associated SNVs were 4 missense base transitions.  No missense mutations were identified in controls.  The importance of the mutations associated with AD and the SNVs that were prevalent in controls, will be discussed and the influence of mtDNA SNVs on AD risk presented.

Speaker- Eli Michaelis, MD, PhD

Dr. Michaelis’ area of expertise is in molecular and cellular neuroscience, brain biochemistry, and brain genomics.  The focus of his research has been on molecular pathways related to conditions that lead to brain degeneration, such as alcoholism, epilepsy, ischemia, aging, or neuro-degenerative diseases, e.g., Alzheimer’s disease. He has performed administrative duties at various levels within the University of Kansas, including Chairmanship of the Department of Pharmacology and Toxicology, Directorship of the Neuroscience Graduate Program, and Directorship of the Higuchi Biosciences Center, a multipdisciplinary center in biomedical sciences.