Pragati Singh
Alzheimer's Disease (AD) is the leading cause of impairment among people over the age of 65 across the world. Amyloid (A) peptide deposition abnormalities, the intracellular buildup of hyperphosphorylated protein neurofibrillary tangles, and dementia are all symptoms of Alzheimer's disease. The neurotoxic oligomer A peptide, which is the disease's neuropathological diagnostic criteria, and protein are mediators of neurodegeneration, which is one of the primary causes. However, oxidative stress, which is defined as an imbalance between antioxidants and oxidants that favours oxidants, is the primary cause and aggressor of these symptoms. Increased free radicals or a reduction in antioxidant defence can cause this imbalance. Free radicals are species with one or more unpaired electrons in their outer shell. Understanding the pathophysiology of Alzheimer's disease is becoming more focused on oxidative balance. Oxidative damage has been seen in both characteristic diseases (senile plaques and neurofibrillary tangles) and normal-appearing pyramidal neurons in the brains of Alzheimer's patients. While this shows that oxidative stress is a proximal event in the aetiology of Alzheimer's disease, the mechanisms by which redox equilibrium is disrupted in the illness are unknown. Determining which of the proposed sources of free radicals, such as mitochondrial dysfunction, amyloid-L-mediated processes, transition metal accumulation, and genetic factors like apolipoprotein E and presenilins, are responsible for redox imbalance will help researchers better understand Alzheimer's disease pathogenesis and develop new therapeutic approaches.