β-adrenergic receptor, amyloid β-peptide, and Alzheimer's disease

This chapter discusses the β-adregenic receptor (βAR), amyloid β peptide, and Alzheimer's disease (AD). Studies in vitro and in vivo have shown that soluble oligomeric amyloid beta (Aβ) peptides are cytotoxic and induce synaptic degeneration and dysfunction that contributes to the pathophysiology of AD in early stage. Accumulating evidence indicates that central nervous system (CNS) noradrenergic system plays an essential role in AD and may mediate and facilitate the detrimental cellular effects of soluble Aβ peptides. Recent studies have revealed direct regulation between CNS noradrenergic system and amyloidogenesis. AD is a progressive neurodegenerative disease and the most common form of dementia affecting more than 35 million people worldwide. AD is characterized by cognitive failure associated with pathology, including cerebral senile plaques containing Aβ peptide, cerebral intraneuronal neurofibrillary tangle of tau protein, neuron and synapse loss, and neurotransmission changes. The works on familial AD form the bedrock of the amyloid cascade hypothesis, which holds that an increase in Aβ may trigger AD.