Dementia is defined as a condition of deteriorated mentality often with emotional apathy. The advance of AD is plotted by stages, from early, mild forgetfulness to severe dementia. The first signs of AD generally appear after the age of 60. These first signs often include loss of recent memory, faulty judgment, and changes in personality. As the disease progresses individuals with AD may forget how to do simple routine tasks such as dressing or bathing. Gradually, they lose all ability to reason and become dependent on caregivers for tending and treatment. In the final stages of the disease patients are bedridden and frequently develop coexisting illnesses. Most commonly, people with AD die from pneumonia.

Alzheimer’s Disease research has been divided into three broad categories; causes and risk factors, diagnosis, and treatment.

Research into the structure and function of the aging nervous system is key to understanding the pathology of the AD brain. Current research into the causes and risk factors in AD are focused on understanding the loss of communication between neurons and the death of neurons in the AD brain. Diagnosis research is looking for ways to identify markers (indicators) of dementias, develop and improve ways to test patients, determine causes and assess risk factors, and improve methods for finding cases and sampling populations. In terms of treatment, researchers are working to slow AD's progression, delay its onset, or eventually, prevent it altogether. Emphasis also is being given to developing ways to improve a patient's ability to function, and to support caregivers of people with AD.

• Amyloid plaques
  The popular "amyloid hypothesis” proposes that abnormal processing of amyloid precursor protein (APP) yields a fragment called beta-amyloid. The beta-amyloid accumulates with other associated proteins and non-neurons to form dense deposits that aggregate by stages into the amyloid plaques that are one hallmark of Alzheimer’s pathology. Advocates of the “amyloid hypothesis” attribute production and aggregation of beta-amyloid as the key event in nerve cell disfunction and cell death. Beta-amyloid may cause inflammation in the brain or may generate free radicals, both of which could eventually lead to neuron toxicity. Other pathways by which beta-amyloid could be toxic to neurons have been proposed. One of these may be the disruption of potassium channels. Ultimately toxic levels of amyloid protein build up in the brain and destroy regions in proximity to the plaque sites.
• Neurofibrillary tangles
  The second most prominent Alzheimer’s theory assigns a causative role to neurofibrillary tangles. Neurofibrillary tangles are insoluble twisted fibers that build up inside neurons. In AD tau, a protein that normally helps organize and stabilize a cell’s internal skeleton, deforms and loses its ability to support the cell, eventually aggregating into neurofibrillary tangles. Although no therapies targeting tau have reached clinical trials, many experts remain convinced that understanding tau will reveal crucial clues about Alzheimer’s devastating effects on nerve cells as well as chemical steps vulnerable to intervention. One study, conducted at the New York State Institute for Basic Research in Developmental Disabilities on Staten Island and New York University Medical Center in New York City, found neurofibrillary changes in 43 to 71 percent of these neurons in people who died of AD as opposed to only 6 percent in the normal population. When they examined the loss of neurons, they found a similar results. This suggests that the formation of tangles and the loss of neurons progresses over the course of AD.

• Familial AD
  Familial AD(FAD) is a rare form of AD, affecting less than 10 percent of AD patients. It is associated with gene mutations on chromosomes 1, 14, and 21. In 1992 researchers at the University of Washington Alzheimer's Disease Center (ADC) in Seattle, supported by NIA and the National Institute of Neurological Disorders and Stroke (NINDS), discovered a link between FAD cases and genes in a particular region of chromosome 14. They were then able to identify the defective gene which they named presenilin 1. Many cases of FAD are caused by presenilin 1. In FAD, all offspring in the same generation have a 50/50 chance of developing AD if 1 of their parents had it. FAD occurs in younger people (usually before age 60) than sporadic AD does. Almost all FAD known so far has an early onset and tends to progress more quickly than the late-onset form of AD.
• Sporadic AD
  Sporadic AD is far more common than FAD. It generally occurs later in life and appears to be related to the apoE gene found on chromosome 19. ApoE comes in several different forms or alleles, but three occur most frequently. People inherit one allele (apoE2, apoE3, or apoE4) of the apoE gene from each parent. Having one or two copies of the E4 allele increases a person's risk of getting AD. Having one or two E4 alleles of the apoE gene increases a person's risk of AD, but not to 100 percent. AD researchers are studying people who inherit different forms of this gene to learn more about risk factors for AD. Scientists have yet to determine the exact degree of risk of AD for any given person based on apoE status.