UPDATE ON “ROAD TO CURE PARKINSON’S” PROJECT

Research“…Realizing that there is a very thin line between Parkinsons and AlzheimersSMART Molecules to address the medical need for Parkinsons disease Dementia.

In April we proudly introduced the scientists and their incomparable history-making work on the PARKINSONS ROAD TO THE CURE. While this remarkable science continues we provide their comparison of Parkinson’s disease Dementia to Alzheimer’s as they continue reporting their progress. We invite you to contact us or them if you want information about supporting or investing in the Parkinsons Road to the Cure. We would be proud to make this important introduction and we continue to salute our scientists as they forge ahead!

Connection of Parkinsons disease with Tau- and Amyloid-Proteins Parkinson’s disease is the second most common neurodegenerative disorder, next to Alzheimer’s disease. Parkinson’s is typically associated with neuronal loss in the substantia nigra and deposits, known as Lewy bodies, containing the synaptic protein α-synuclein (α-Syn) in the cell bodies. Mutations and multiplications of α-Syn are linked to hereditary forms of the disease. These genetic abnormalities tend to exacerbate the propensity of α-Syn to misfold and aggregate, which have a direct role in Parkinson’s pathogenesis. Postmortem studies on the brain tissues from Parkinson’s patients have confirmed the presence of insoluble, fibrillar forms of α-synuclein [Nature, 388, 839 (1997)]. Several experimental models provide additional support for the role of α-Syn aggregation in neurodegeneration. For example, overexpression of the Ala53Thr mutant variant of α-Syn in transgenic mice led to the formation of α-Syn immunoreactive deposits resembling Lewy body pathology as well as cognitive and motor clinical phenotype and reduced survival time. Furthermore, suppression of Ala53Thr α-Syn expression resulted in a decrease in neuro-pathology and clinical symptoms [J. Neurosci., 31, 10076 (2011)].

Most Parkinson’s patients exhibit some level of cognitive dysfunction, including dementia, referred to as Parkinson’s disease Dementia (PDD), during the course of their illness. Cognitive impairment is a common feature of Parkinson’s and may be a natural consequence of end-stage disease. Overall prevalence of cognitive impairment in Parkinson’s is roughly 30%, and ~80% of longitudinally followed patients with Parkinson’s develop dementia over the course of the disease. Dementia in Parkinson’s patients is estimated to be at least fourfold higher than it is in the general public. Also, patients with PDD experience dementia for an average of 3-4 years during their disease course. Thus, cognitive dysfunction and dementia have serious implications for patient quality of life, public health and the cost of care.

Neuropathology Underlying PDD

α-Synuclein Involvement In general, cortical Lewy body is more extensive and severe in PDD than in Parkinson’s without dementia. Several lines of evidence from studies using α-Syn immunohistochemistry implicate cortical α-Syn pathology as the strongest correlate of dementia in PDD. Most large studies have found that PDD cases have higher levels of cortical α-synuclein than do cases of Parkinson’s without dementia [(Neurology, 54, 1916 (2000)]; Ann Neurol., 72, 587 (2012)].

Amyloid Plaque and Tau Neurofibrillary Tangles (NFTs) Involvement Recently, two studies have shown that Parkinson’s patients with sufficient numbers of NFTs and amyloid-plaques (Aβ-plaques) have clinical dementia and hence could be assigned a diagnosis of PDD plus Alzheimer’s [Ann Neurol., 72, 587 (2012); Brain, 134, 1493 (2011)]. One of these studies found that a regression model incorporating cortical α-Syn, Tau and Aβ pathologies together more accurately predicted dementia than single marker alone. Thus, Alzheimer’s neuropathology appears to have an important role in the pathogenesis of PDD for a significant proportion of patients.

What ICB International (ICBI) is doing to address the Pathogenesis of PDD

Realizing that there is a very thin line between Parkinson’s and Alzheimer’s, ICBI scientists have already developed α-Syn- and Aβ-SMART Molecules to address the medical need for PDD. Currently, its scientists are developing Tau and phosphor-Tau SMART Molecules. With appropriate funding ICBI intends to make available to the patients its unique therapeutic drug comprising of three drugs on the same molecule to neutralize the toxic effects of α-Syn, Tau and Aβ pathogens to promote healthy environments for proper functioning of neurons in the brains.

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