Foreword

Alzheimer's disease (AD) is the most common cause of age-related dementia, accounting for up to 70% of all dementia cases. There are 50 million individuals living with AD worldwide and its global prevalence is expected to grow due to predicted expansion of the older population. AD presents with irreversible cognitive decline, which commences as insidious short-term memory dysfunction and gradually spreads to other cognitive domains, rendering patients mute and non-ambulatory after 10-15 years of progressive course. AD is a genetically complex disease. The majority of AD cases are sporadic, and their risk is predominantly controlled by the APOE genotype. The APOE e4 allele increases AD risk in allele-dose dependent fashion while the e2 allele has a risk-mitigating effect. Early-onset familial AD (FAD) accounts for 2-5% of all AD cases and is caused by mutations  of the amyloid precursor protein (APP) or presenilin 1 (PS1) or 2 (PS2) genes, which are inherited in autosomal dominant fashion. Neuropathological hallmarks of AD include accumulation of insoluble β-amyloid (Aβ) peptides in the form of parenchymal plaques and vascular deposits, intraneuronal neurofibrillary tangles (NFTs) composed of misfolded and hyperphosphorylated microtubule-associated τ protein, activated astrocytes and microglia and widespread loss of synapses and nerve cell bodies. Unfortunately, there are neither effective preventive measures nor efficacious treatments available for this devastating disease.  CONTINUE READING…..