Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-beta (Aβ) plaques and neurofibrillary tangles, leading to the loss of neurons and cognitive decline. The disease is influenced by both genetic and environmental factors, with mutations in the amyloid precursor protein (APP) and presenilin genes playing a significant role. Aβ is produced through altered proteolytic processing of APP, and its accumulation is linked to oxidative stress, impaired energy metabolism, and disrupted calcium homeostasis. These factors contribute to synaptic dysfunction and neuronal death. While there is no cure for AD, research is advancing towards preventative and therapeutic strategies, including lifestyle modifications, dietary changes, and immunotherapies targeting Aβ. Studies suggest that cognitive stimulation, physical exercise, and diets low in saturated fats may reduce AD risk. Immunization against Aβ has shown promise in animal models, with some clinical trials indicating potential benefits. However, challenges remain in translating these findings to human applications. Glial cells, including microglia, play a complex role in AD, contributing to both neurodegeneration and potential protective mechanisms. Ongoing research aims to develop targeted therapies that address the underlying pathogenic processes, such as amyloid clearance and modulation of inflammatory responses. Despite progress, AD remains a significant public health challenge, requiring further investigation into its molecular mechanisms and effective interventions.Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-beta (Aβ) plaques and neurofibrillary tangles, leading to the loss of neurons and cognitive decline. The disease is influenced by both genetic and environmental factors, with mutations in the amyloid precursor protein (APP) and presenilin genes playing a significant role. Aβ is produced through altered proteolytic processing of APP, and its accumulation is linked to oxidative stress, impaired energy metabolism, and disrupted calcium homeostasis. These factors contribute to synaptic dysfunction and neuronal death. While there is no cure for AD, research is advancing towards preventative and therapeutic strategies, including lifestyle modifications, dietary changes, and immunotherapies targeting Aβ. Studies suggest that cognitive stimulation, physical exercise, and diets low in saturated fats may reduce AD risk. Immunization against Aβ has shown promise in animal models, with some clinical trials indicating potential benefits. However, challenges remain in translating these findings to human applications. Glial cells, including microglia, play a complex role in AD, contributing to both neurodegeneration and potential protective mechanisms. Ongoing research aims to develop targeted therapies that address the underlying pathogenic processes, such as amyloid clearance and modulation of inflammatory responses. Despite progress, AD remains a significant public health challenge, requiring further investigation into its molecular mechanisms and effective interventions.