AD is part of a group of disorders, termed dementias, that are characterized by cognitive and behavioral problems. AD advances progressively, from mild forgetfulness to a severe loss of mental function. In most people with AD, symptoms first appear after age 60. The earliest symptoms characteristically include loss of  recent memory, later compounded by faulty judgment, and changes in personality. Often, people in the initial stages of AD think less clearly and tend to be easily confused. Later in the disease, they may forget how to do simple tasks, such as how to dress themselves or eat with proper utensils. Eventually, people with AD lose the capacity to function on their own and become completely dependent on other people for their everyday care. Finally, the disease becomes so debilitating that patients are bedridden and likely to develop other illnesses and infections. Most commonly, people with AD die of pneumonia.

Although the risk of developing AD increases with age, AD and dementia symptoms are not a part of normal aging. AD and other dementing disorders are caused by diseases that affect the brain. In the absence of disease, the human brain often can function well into the tenth decade of life.

Alzheimer's disease (AD) is the most common cause of dementia that arises on a neuropathological background of amyloid plaques containing -amyloid (A) derived from amyloid precursor protein (APP) and -rich neurofibrillary tangles. To date, the cause and progression of both familial and sporadic AD have not been fully elucidated. The autosomal-dominant inherited forms of early-onset Alzheimer's disease are caused by mutations in the genes encoding APP, presenilin-1 (chromosome 14), and presenilin-2 (chromosome 1). APP is processed by several different proteases such as secretases and/or caspases to yield Aand carboxyl-terminal fragments, which have been implicated in the pathogenesis of Alzheimer's disease. Alzheimer's disease and Parkinson's disease are associated with the cerebral accumulation of A and -synuclein, respectively. Some patients have clinical and pathological features of both diseases, raising the possibility of overlapping pathogenic pathways. Recent studies have strongly suggested the possible pathogenic interactions between A, presenilins, and/or -synuclein. Therefore, treatments that block the accumulation of A and -synuclein might benefit a broad spectrum of neurodegenerative disorders. This review covers the trafficking and processing of APP, amyloid cascade hypothesis in AD pathogenesis, physiological and pathological roles of presenilins, molecular characteristics of -synuclein, their interactions, and therapeutic strategies for AD.

-Most common form of dementia

-Disease characterized by progressive loss of memory

-Ultimate result is total degradation of intellectual and mental activities.

-Affects 10% of people over age 65

-Affects 30-35% of people over age 85

Its neuropathological characteristic includes:

-Senile plaques: associated with beta amyloid peptide

-Neurofibrillary tangles (NFT): contain hyperphosphorylated forms of

-microtubule associated protein tau.

-Loss of neurons in hippocampus