Synaptic Of Alzheimer 's Disease Essay

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and synapses to prevent amyloidosis and inhibit further aggregation56. In the CNS, nonneuronal cell linages like astrocytes have been reported to have an elevated level of HSPs to target misfolded protein degradation53. However, a major gap in the field is the lack of any such reports about the extracellular chaperons in the protection of CNS and neuronal structure and function.

Although not fully understood, but it has been reported that different cells have different susceptibility to proteotoxic stress. The unfolded protein response evoked by cells in response to proteotoxic stress involves an orchestered functioning of the proteostasis pathways57.
Neuronal cells and cell of the central nervous system bear an increased risk of being burdened by misfolded protein aggregates under stress or disease conditions. For example, dopaminergic neurons in the substantia nigra in case of Parkinson’s disease, motor neurons in the motor cortex and spinal cord in amyotrophic lateral sclerosis, cholinergic neurons in the hippocampus and entorhinal cortex in case of Alzheimer’s disease, are those cells with greater susceptibility in comparison to other cells51. One way of looking at this is to explore the difference in terms of the expression of the proteostasis components in these cells, and that of the pathological marker proteins like amyloid-β, α-synuclein, Lewy body, huntingtin and bunnina bodies51. A comparison of deficiencies or abnormal expression pattern of proteostasis
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