Abstract
One of the most prevailing conditions of dementia is the illness known as Alzheimer's disease. The diagnostic signs of Alzheimer's disease progressively get worse over a long period since it is a cumulative condition. Alzheimer's disease causes modest memory loss in its initial stages, but people cannot converse or react to their surroundings in the later stages of the disease. In Alzheimer's disease, the destruction of neurons and the interconnection between them in the cortical region and the hippocampus is the beginning, after which the disease proceeds. The cerebral cortex regions are subsequently involved in thinking, linguistics, and interpersonal communication. Other parts of the brain eventually suffer harm as well. A person with Alzheimer's slowly loses the capacity to live and do daily tasks on their own over time. The illness is lethal in the end. Dementia is most commonly caused by ageing. Although dementia grows more prevalent as individuals age, this does not imply that dementia is a natural component of ageing. Up to 40% of those over 85 years who have dementia suffer from this condition. Amyloid, a beta protein that wrongly builds up and creates neurofibrillary tangles in the brain, causes Alzheimer's, a condition of protein misfolding. According to tradition, the primary cause of neuronal degeneration caused by the amyloid hypothesis is the buildup of beta-amyloid peptides. According to theory, the hazardous protein form that upsets the cell's calcium ion balance clumps amyloid fibrils, which leads to apoptotic cell death. This review article discusses the pathophysiology and biochemistry of various neuroprotective proteins to examine the potential of future anti-medications for Alzheimer's disease.