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Dementia 2016
September 29-October 01, 2016
Volume 6 Issue 5(Suppl) J Alzheimers Dis Parkinsonism 2016
ISSN:2161-0460 JADP, an open access journal
conferenceseries .com
September 29-October 01, 2016 London, UK
5th International Conference on
Alzheimer’s Disease & Dementia
Heejin Park, J Alzheimers Dis Parkinsonism 2016, 6:5(Suppl)
Role of presenilin-1 mutations in Mitochondrial dynamics
Heejin Park
Sungkyunkwan University, Republic of Korea
Early stage of Alzheimer's disease reveals mitochondrial deficit and dysfunction. Mitochondrial dysfunction in Alzheimer's
disease causes synaptic alteration, imbalance of lipidhomeostasis, calciumhomeostasis, and lackofATPproduction. Familial
Alzheimer's disease-linked Presenilin-1, catalytic subunit of γ-secretase, mutations cause early onset Alzheimer's disease. All
mutation types have different pathological mechanism and ultimately break down cellular homeostasis. Our research shows
more details about relationship between Presenilin-1 mutations (PS1A431E, PS1E280A, PS1H163R, PS1M146V, PS1ΔE9) and
mitochondrial dysfunctions. All of PS1 mutants-expressing cells exhibited mitochondrial dysfunctions and reduced levels of
proteins involved in mitochondrial dynamics without alteration of total mitochondrial biogenesis.
Biography
Heejin Park is studying at Molecular Cell Biology laboratory, from Sungkyunkwan University School of Pharmacy, South Korea, for her M.S. Course. She completed
her bachelor degree from the Department of Genetic engineering of Sungkyunkwan University and decided to transfer to School of Pharmacy because she was
interested in neurodegenerative diseases and Alzheimer’s Disease. Now she is investigaing for the relationship between mitochondrial dysfunction and Alzheimer's
Disease.