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Volume 8 Journal of Alzheimers Disease & Parkinsonism
ISSN: 2161-0460 Dementia 2018
October 29-31, 2018
Page 50
conferenceseries.com
October 29-31, 2018 | Valencia, Spain
12th International Conference on
Alzheimer’s Disease & Dementia
Mourad Tayebi, J Alzheimers Dis Parkinsonism 2018, Volume 8
DOI: 10.4172/2161-0460-C7-053
Investigating age-related dementia in natural higher mammalian models
Proteinopathies such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are a group of disorders thought to be caused by
abnormal folding or misfolding of beta amyloid (Ab) and α-synuclein, respectively. Their pathogenesis is not well understood
due to unresolved molecular mechanisms. This is further complicated by the lack of proper natural disease models that might
be effective in aiding the investigation of the molecular mechanisms underlying these disorders. Dogs spontaneously deposit
human-type Ab as they age and thus are a natural higher mammalian model of aging. The canine Aβ precursor protein (APP)
is virtually identical to human APP. Previous studies demonstrated that aging dogs spontaneously accumulate human-type Aβ
and parallel declines in cognition. Further, the outcomes of immunotherapy studies in aged dogs has predicted human clinical
trial outcomes; clearance of Aβ plaques with little cognitive benefits. In more recent work, we show that canine derived Aβ
was toxic to human neuronal cell lines and led to aggregation of human Aβ. Eastern grey kangaroos (EGK) display a typical
movement disorder presentation associated with grass phalaris poisoning. We show that this disorder, known as phalaris staggers
displays a parkinsonian type syndrome with associated Parkinson’s-like signs and neuropathology, including synucleinopathy and
neuromyopathy. Studies of proteinopathies have typically used transgenic mouse models and subsequently translated to human
clinical trials. However, the success rate of these translational studies has been limited and unfortunately resulted in negative
outcomes and some with adverse events. It is critical to identify and validate natural higher mammalian models of proteinopathies
to investigate the molecular mechanisms underlying these disorders and test therapeutic outcomes prior to translation to human
clinical trials.
Biography
Mourad Tayebi is an Associate Professor in Biomedical Sciences at the School of Medicine at Western Sydney University, Australia. He is an International Expert in
the field of protein misfolding diseases, with specific focus on investigating the molecular mechanisms underlying pathogenic protein misfolding and characterizing the
misfolding associated with these disorders. His team is very active in the development of early blood diagnostic test screen for Alzheimer’s and effective therapies for
neurodegenerative diseases.
Mourad Tayebi
Western Sydney University, Australia
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