Oxidative damage to proteincoding RNA or noncoding RNA will, in turn, potentially cause errors in proteins andor dysregulation of gene expression. As a consequence of peroxidations of lipids, proteins, RNA and DNA, high levels of ROS cause damage to various cellular components and ultimately result in cell death.A hallmark of AD pathology is brain atrophy, subsequent to gradual cell loss in the CNS.Characteristic neurofibrillary tangles and neural plaques are seen post mortem.PD is another CNS neurodegenerative disease afflicting millions of the older population, with most cases occurring after the age of. Early on in the course of the disease, the most obvious symptoms are movementrelated, including tremor, rigidity, slowness of movement and difficulty with walking and gait.The motor symptoms of PD result from the slow degeneration of dopaminegenerating neurons in the substantia nigra of the basal ganglia, a region of the midbrain, leading to progressive loss of muscular coordination and balance. Later, thinking and behavioral problems may arise, with dementia commonly occurring in the advanced stages of the disease, whereas Olmesartan depression is the most common psychiatric symptom.Other symptoms include sensory, sleep and emotional problems.HD characterized with abnormal involuntary writhing movements called chorea is a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and psychiatric problems.Although physical symptoms of HD can begin at any age from infancy to old age, it usually begins between and years of age.Medical imaging techniques such as computerized tomography can show atrophy of the caudate nuclei and striatal volume in the disease. Under normal conditions, a transmembrane protein amyloid precursor protein is critical to neuron growth, survival and postinjury repair. However, in AD, APP is cleaved into a small peptide, amino acids in length, called A, by enzymes through proteolysis. A forms clumps and deposits outside neurons in dense formations known as senile plaques. All humans have two copies of the huntingtin gene is an aggregateprone protein.During the natural clearance process of cells, these proteins are retrogradely transported to the cell body for destruction by lysosomes.Under pathological conditions, these mutant proteins aggregate and damage the retrograde transport of important molecules such as BDNF by damaging molecular Olmesartan motors as well as microtubules, causing pathological changes and disease symptoms.Prior to the destruction in ALS, motor neurons develop proteinaceous inclusions in their cell bodies and axons.Protein degradation pathways play a crucial role in removing misfolded proteins and preventing protein aggregation.ROS mediate neurotoxicity in each of these diseases through modifying the hallmark protein by oxidation.A found in senile plaques is considered to have a causal role in AD.HO at M results in an increase in the levels of intracellular A in human neuroblastoma SHSYY cells. Oxidative stress results in accumulation of potentially neurotoxic A peptide by inducing the amyloidogenic process of APP and increasing the activity of secretase. Cerebral amyloid angiopathy is associated with most cases of AD, characterized by A deposits in brain vessels. TDP is the major disease protein in ubiquitinpositive inclusions of ALS.Accumulation of insoluble TDP aggregates could impair normal TDP function and initiate disease progression.

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