The Roles of Genetics in Aβ related Alzheimer's Diseases

About 35 million people worldwide were suffered from Alzheimer’s disease (AD) in 2014 and the number of patients was expected to increase by 4-fold in 2050. As a neurodegenerative disease impacting our society, the pathogenesis and prognosis of AD have not yet fully understood. Senile plaque is generally regarded as one of the hallmarks of the disease, which may be due to the imbalance of Aβ peptides in the brain. Over the last decades, studies of early onset familial AD have led us to a deeper understanding of the genetics and molecular biology of AD. There is increasing evidence to suggest that the pathogenesis of AD is more likely to be caused by multiple genetic mutations. However, the precise genetic component leading to AD pathogenesis remains unclear. In this review, we will briefly introduce the classification of AD in the context of genetics. Then we will discuss the gene mutations in chromosome 21, 19 and presenilin as well as their links to Aβ peptides. Imaging data will be discussed alongside to complement the associated structural and physiological changes in the brain. It is our hope that future research in genetics will continue to enhance our understanding of the pathogenesis of AD and the mechanisms leading to the formation of senile plaques.