Molecular mechanisms and genetics of Alzheimer’s disease

Abstract

Dementia is mostly caused by neurodegenerative diseases like Alzheimer’s disease (AD). AD is the most common form of dementia. It is caused by both genetic and environmental factors. Due to neuronal death in a number of brain regions, including the hippocampus, entorhinal areas, temporal lobe, and cingulate cortex, AD causes memory loss and gradual cognitive impairment. The condition’s two main pathogenic components are intracellular neurofibrillary tangles created by clusters of hyperphosphorylated tau protein and amyloid plaques made up of extracellular amyloid (Aβ) peptide aggregates. In contrast to the APOE- ε4 allele, which was found to have a significant impact on late-onset AD, presenilin 1, presenilin 2, amyloid precursor protein were genetic risk factors that were causal for early-onset AD. Misfolded proteins accumulate within the neuron, causing prolonged cellular stress in AD, a progressive neurodegenerative disease. Neurofibrillary tangles and senile plaques are two of the neuropathological hallmarks of Alzheimer’s disease that lead to the destruction of synapses and the death of neurons. AD is mostly caused by the death of nerves, particularly cholinergic nerves. In the absence of these cholinergic neurons, acetylcholine levels fall. This review discusses key genes involved in the pathogenesis and pathophysiology of AD, as well as the disease’s molecular mechanisms.

Keywords

• alzheimer’s disease
• apolipoprotein e
• app
• neurodegenerative disease
• pathogenesis
• presenilins