Type 2 diabetes (T2D) and neurodegenerative diseases (NDs) are commonly associated with growing age. They have drawn significant attention due to their rise at an alarming rate. The increasing occurrence of both these diseases has lead to a great socioeconomic burden as well as major public health concerns worldwide. NDs include a range of disorders, which involves dysfunction of the central nervous system (CNS), due to degeneration of neurons and associated pathological processes. These diseases include Lewy body dementia, vascular dementia, Huntingtonâs disease, Parkinsonâs (PD), and Alzheimerâs diseases (AD). Interestingly, in spite of different pathophysiology of these neurodegenerative diseases, there are some common similarities between these neurodegenerative disorders namely atypical protein assemblies as well as induced cell death. Hence, most of the neurodegenerative disorders are characterized by the inappropriate aggregation of amyloidic proteins, such as AÎ² peptides derived from Amyloid precursor protein (APP) and paired helical filament (PHF) aggregates of microtubule-associated protein (MAP), tau, which are known respectively as senile plaques and neurofibrillary tangles in the context of AD. Other pathological examples of abnormal protein aggregates include PHF tau in tauopathies and frontotemporal dementias, huntingtin proteins in HD, Î±-synuclein in PD, and filamentous prion proteins in CreutzfeldtâJakob disease (CJD). T2D is characterized by hyperglycaemia, insulin resistance or relative lack of insulin insulin is secreted by Î²-cells but in T2D it fails to stimulate glucose uptake by the cells and hence it is called insulin independent diabetes.
Global Current Trends in Drug Designing for Management of Type-2 Diabetes and Neurodegenerative Disorders: Haque A, Alam Q, Alam MZ and Kamal MA
Last date updated on July, 2014