Role of myosins in neurodegeneration, including Parkinson and Alzheimer diseases

Parkinson | Parkinsons 2016 | Role of myosins | USA | Worldwide Events | Europe | Asia | Middle East | 2016

Omics Group Conference Series would like to welcome all the Directors, Heads, Deans, Professors, Scientists, Researchers, Doctors and students of neurology department  for “2nd  International conference on Parkinson's Disease and Movement Disorders” on December 05-07, 2016 at Phoenix, USA, The theme of Parkinson conference is based on “Leading Innovation and Remedial Insight of Parkinsons Disease”. This conference is mainly focus will focus the latest and exciting innovations in every area of parkinsons research, and it will offer a unique opportunity for investigators from all over the world to meet, network, and perceive new scientific interactions.

Parkinson’s disease is one of the commonest neurological conditions. It is estimated to affect up to 160 per 100,000 of the general population with an annual incidence of 15–20 per 100,000. Many population studies have shown the rising prevalence with age (up to 2% of the population aged 80 and over). Around 1 in 7 cases are diagnosed below the age of 60 years. The costs of treatment have been estimated at between £560,000 and £1.6 million per 100,000 of the population.

In USA a 3-year prospective study of the economic cost of PD was performed in 2006. The average annual cost per patient was estimated at $12,091, of which 55,9% accounted for direct costs. Drugs took up the major share of direct costs, $5,763 per year. Indirect costs accounted for $4,851 per patient per year. Within this, 76% of the costs were related to nursing care and the loss of productivity.

Myosin5a (Myo5a) is an actin-dependent motor protein that is highly expressed in the brain, and involved in vesicular/organelles transport and its absence leads to movement disorders in humans and animal species (Griscelli and Elejalde syndromes in humans), rodents (dilute lethal phenotype in mice, and diluteopisthotonus of Wistar rats), and Arabian horses Lavender Foal Syndrome.
A spontaneous autosomal recessive rat model for neurodegeneration caused by a mutation in the Myo5a gene was developed in our laboratory. The pleiotropic effects of this mutation affect the coat color, central nervous and neuroendocrine systems.
Preliminary data from our model of Myo5a mutant Berlin-Druckrey (BD-IV) “shaker” rats demonstrated marked alterative changes involving the alpha-synuclein (α-syn) overexpression, decrease dopamine (DA) levels, alteration of DA metabolism, and overexpression of tau protein in specific anatomical areas of brain in shaker rats compared with non-affected siblings. The movement disorder and alterative biochemical changes increased in severity after 15 days postnatal. The mechanisms responsible for neurological phenotypes in the deficient Myo5a affected animals are less understood and deserve further investigation. Possible role of diverse myosins in synaptic transmission or plasticity has not been investigated. Similar neurological degenerative changes are common in human neurodegenerative diseases such as
Alzheimer, Parkinson’s, and Lewis Body dementia, which make this animal model ideal for
mechanistically investigating human diseases with potential development of novel therapy, which can lead to translational studies. The main challenge for the future will be to investigate the molecular mechanisms of Myo5a neurodegeneration and its interaction with other proteins underlying its functions.