Alzheimer's Disease


Alzheimer's disease (AD) is the most common form of dementia in people aged 65 years and older. It is an irreversible and incurable progressive neurological disease resulting from degeneration and eventual death of large numbers of neurons (nerve cells) in several areas of the brain, accompanied by diminished brain size. Although AD onset is typically after age 65, middle-aged adults are diagnosed in rare instances. The condition begins with short-term memory loss and is followed by slow, progressive loss of long-term memory. The loss of cognitive and intellectual functions leads to the deterioration of physical functioning and eventual incapacitation. Although AD had no known cure as of 2017, results of research studies indicated that staying physically and mentally active into older adulthood can help to reduce risk of developing AD and other forms of dementia, and physical exercise is highly recommended in older adults already diagnosed with AD.

Positron emission tomography (PET) scans showing a normal brain, an impaired brain, and a brain affected by Alzheimer's disease.

Positron emission tomography (PET) scans showing a normal brain, an impaired brain, and a brain affected by Alzheimer's disease. Alzheimer's is the most common form of dementia in people aged 65 years and older, and is currently an irreversible and incurable disease.
(Science Source)

Alzheimer's disease. The progression of neurofibrillary tangles that spread throughout the brain is shown in purple. Plaques also spread throughout the brain until tissue is severely damaged and shrunken (final stages of the disease).


AD is an insidious form of dementia that gradually robs people of their memories and cognitive abilities, leading eventually to physical decline. The disease is characterized by four major cognitive deficits:

The Alzheimer's Association states that the precise cause of AD remained unknown as of 2017; even though progressive brain cell failure is known to be responsible for AD symptoms, it is still unclear why brain cells fail. Some experts suggest that a complex interaction of multiple factors is responsible, including older age, a family history of AD, and having a specific allele of the apolipoprotein E gene (APOE-e4). Additionally, specific so-called designer proteins created in the laboratory (amyloid-abeta proteins) are similar to the proteins found in AD patients, and the tendency of these proteins to stick together in clumps between neurons in the brain may result in the cell death and cognitive decline seen in AD. Studies of AD patients show that brain inflammation and restriction of blood flow to the brain may contribute to the development of beta-amyloid plaques and neurofibrillary tangles. These plaques and tangles found in the brains of AD patients at autopsy are considered the hallmarks of AD. The plaques, sometimes called senile plaques, are sticky clumps or clusters of dead and dying neurons and other cellular debris surrounding insoluble deposits of beta-amyloid. The latter are fragments of a larger protein called amyloid precursor protein (APP) that was processed improperly. Scans that visualize brain activity have also shown that dementia plaques attack the brain's language centers.

Studies have also demonstrated that exercise exercise is the most powerful tool available to keep both the body and brain in good shape and to help older adults maintain healthy physical and mental status as long as possible. Regular exercise is recommended not only for healthy adults but for those already diagnosed with AD; exercise has been shown to help AD patients retain mental and physical functioning longer during the disease course.


AD is the most common degenerative brain disorder in populations around the world and was believed to be escalating rapidly as of 2017. In the United States, the number of AD patients aged 65 and older is expected to triple by 2050, ranging from 13 to 16 million older adults. AD accounts for 50%–70% of all cases of dementia in the United States and for about 75% of all dementias in people over age 65. In 2017, 5.4 million Americans of all ages were estimated to have AD; of these, 5.2 million were age 65 and older. The exact number was difficult to determine since AD is often misdiagnosed or not diagnosed until the disease is in an advanced stage. It is the sixth leading cause of death among all U.S. adults after heart disease, cancer, chronic lower respiratory disease, accidents, and stroke; and the fifth leading cause of death among people aged 65 and older. While deaths from other major diseases decreased between 2006 and 2016, AD deaths increased significantly. About 84,000 people with AD died in 2013, and an estimated 700,000 individuals were predicted to die of the disease in 2016. The mortality rate was twice as high in AD patients as in older adults without AD.

AD rarely occurs before the age of 60. Earlyonset, also called younger-onset AD, affects adults in their 30s, 40s, and 50s. About 200,000 individuals are younger than age 65 at disease onset in contrast to more than 5 million adults older than age 65 at onset. The incidence of AD is slightly higher among women than among men; women aged 65 and older have a 1 in 6 chance of developing AD in their lifetimes in contrast to a 1 in 11 chance of men developing AD. However, the reported incidence is likely affected by the fact that women tend to live longer. About half of all long-term care patients in the United States have AD.

AD appears to be more prevalent among African Americans, with estimates ranging from 14% to almost 100% higher than the estimated prevalence among Caucasian Americans. One study reported that AD onset in Hispanic individuals is about five years earlier than average onset in Caucasians.

AD incidence in other developed countries is about the same as in the United States. In countries such as Japan with an aging population and a higher percentage of people over age 65, AD incidence is higher than in the United States. In developing countries, the percentage of the population with AD is lower because fewer people live to 65 years. However, more than 50% of people with AD live in developing countries and, by 2025, incidence is expected to be above 70%.

Causes and symptoms


The cause of AD is unknown although researchers have suggested that a combination of genetic and environmental factors are responsible. Contributing factors are identified as older age, a family history of AD, and the presence of specific risk genes such as APOE-e4 or predictive genes. Viral, immunological, and/or biochemical etiologies have also been proposed, but no definitive cause had been identified as of 2017.

Research has explored possible environmental causes. Highly reactive molecules called free radicals damage all types of cells through oxidative processes, especially brain cells that have lower levels of protective antioxidants. Accumulation of free radicals from exposure to environmental toxins may contribute to the development of AD in susceptible individuals.


AD symptoms fall in three categories: cognitive losses affecting primarily memory and learning ability; behavioral and psychiatric symptoms of dementia (BPSD); and difficulties with activities of daily living (ADL). For most of the 20th century, studies of AD patients focused on cognitive symptoms. It was not until the 1980s and 1990s that researchers began to examine behavioral and psychiatric symptoms more closely. All three groups have been studied since the 2010s, and research continued as of 2017.

Symptoms associated with behavioral and psychiatric aspects of dementia (BPSD) include:

Symptoms affecting skill levels of patients with AD, especially personal hygiene and self-care tasks, include difficulties with the following:

Although the rate of AD progression and specific symptoms varies with the individual, the general course of progression is fairly consistent. Research results indicate that different patterns of atrophy in the brain may explain differences in AD symptoms among patients. Nevertheless, early-onset AD often progresses faster than the more common late-onset. The Alzheimer's Association describes three general stages of AD—mild or early stage, moderate or middle stage, and severe or late stage. However, the association and other organizations have adopted the seven-stage expanded definition of AD introduced by Dr. Barry Reisberg of New York University, described as follows:


An early and accurate diagnosis of AD is important for developing strategies for symptom management and treatment, especially because AD patients and their families need to plan for treatment, longterm care, and financial requirements while the patient can still be involved in decision making. A diagnosis of AD also may help family members to avoid unnecessary anger and feelings of impotence when dealing with disease progression.

An AD diagnosis requires identifying slowly progressive dementia, excluding other possible causes for dementia (differential diagnosis), and results of brain-imaging studies that show changes in brain structure, usually in the form of shrinkage. A definitive diagnosis of AD may be complicated by the presence of another disorder, resulting in a diagnosis of possible AD until the symptoms can be fully attributed to AD. Probable AD is diagnosed when physicians and psychiatrists have ruled out all other disorders that could produce similar symptoms. As part of the diagnostic evaluation, healthcare professionals also assess patients' ADL levels to determine how much and what type of care is needed for each AD patient.


First and foremost, developing and maintaining a workable exercise plan for AD patients helps maintain overall health and specific issues associated with the disease. Exercising on a regular basis can improve mobility, balance, and maintain independence for as long as possible. Moderately strenuous exercise has been shown to improve cognitive (thinking) skills in people with AD. Other medical studies have shown that light exercise, such as walking or housework, helps to reduce the incidence of wandering, aggressive behavior, and other problem behaviors.

Physical exercise has also been shown to support the growth of new synaptic connections within the brain that may help maintain brain plasticity. Specifically, neuroplasticity, or brain plasticity, is the ability of the brain to organize its neural pathways based on new experiences. For instance, if part of the brain is damaged, the undamaged portion can learn to do something that was previously performed by the damaged part. In addition, when a person does something different, such as driving to work using a new route, memorizing a new fact, learning a complex board game, or figuring out a puzzle, the brain is being exercised in ways that will help to stave off the symptoms of dementia. In a similar way, physically exercise helps to exercise the brain. To make sure a person with AD receives proper attention, regular visits with a qualified primary care physician, along with periodic visits to specialists and other healthcare professionals, are necessary to ensure that an AD patient receives proper medical attention and supervision of overall health. Having a proper diet and following an appropriate exercise plan are central to care for AD patients.

The mainstay of treatment is establishing daily routines, delivering good nursing care and/or homecare, and providing physical and emotional support. In the initial stages of AD, counselling by a psychologist or participation in an AD support group is recommended. The patient and caregiver are advised to establish a relationship with a primary care provider so that illnesses, especially urinary or respiratory infections, can be promptly diagnosed and treated rather than being simply attributed to the inevitable decline of AD. Neurological and behavioral aspects of AD, including anxiety, agitation, defiant behavior, insomnia, hallucinations, and seizures are typically treated on an as-needed basis. Certain drugs, usually anti-anxiety or anti-psychotic medications, sedatives, and sleep medications, may be used to help manage mood and behavior problems.

As of 2017, effective treatment of AD was an important area of research, and various drugs were being evaluated for their possible neuroprotective effects against beta-amyloid-induced oxidative stress in the brains of laboratory animals. Laser therapies were also being investigated in animal studies as a possible treatment for beta-amyloid toxicity such as that found in AD. Stem cell therapy was another area of investigation for treatment of neurodegenerative diseases such as AD. In addition, the National Institutes of Health (NIH) and other agencies continued to sponsor clinical trials of new drugs and therapies targeting AD.

Exercise has been found to be especially beneficial for AD patients when added to conventional treatment. Regular exercise, including cardiovascular exercise, is highly recommended to increase the endurance and strength of AD patients. Such exercises help to reduce the rate of mental decline; improve behavior (especially reduce the risk of depression and anxiety) and memory; decrease injuries (such as from falls) by improving balance, flexibility, and strength; and enhancing communications and motor skills.

Study results have consistently shown that AD patients who exercise regularly are less depressed than those who do not exercise. In addition, those who exercise have improved abilities to function on a daily basis. Balance exercises are important too. When mental function deteriorates, balance is adversely affected. By performing balance exercises, individuals can reduce or reverse such deterioration, so chance of injury is reduced.

Endurance exercises improve heart rate and respiratory rate function. Examples of endurance exercises include walking, dancing, housework, gardening, yoga, and swimming or aquatic exercises.

Physical exercise helps to improve the clinical condition of AD patients by strengthening their heart, increasing blood flow (especially to the brain), lowering low-density lipoprotein cholesterol (LDL) cholesterol and increasing high-density lipoprotein cholesterol (HDL), and reducing the risk of sickness and injury. Mental exercise, such as reading a book, doing crossword puzzles, playing games, and learning a new skill, all help to keep the brain active and alert. All forms of exercise help to improve the general attitude of AD patients.


Excessive restlessness or emotional disturbance that is often associated with anxiety or psychosis; common in middle-stage AD.
Inability to recognize familiar people, places, and objects.
Partial or complete loss of memory or gaps in memory.
An almond-shaped brain structure of the limbic system that is activated in stressful situations and triggers fear.
A substance that prevents the destructive effects of oxidative chemicals in the body.
Loss of language abilities.
Apolipoprotein E (APOE)—
A protein that transports cholesterol throughout the body. One form of this protein, APOE e4, is associated with a 60% risk of late-onset AD.
An inability to perform purposeful movements that is not caused by paralysis or loss of feeling.
The wasting away of body tissue due to cellular degeneration.
Autosomal dominant—
A gene located on a chromosome other than the X or Y sex chromosomes, whose expression is dominant over that of a second copy of the same gene.
Beta-amyloid plaques—
Senile plaques; structures in the brain, composed of dead or dying nerve cells and cell debris surrounding deposits of beta-amyloid protein, that are diagnostic of AD. Beta-amyloid forms when amyloid precursor protein (APP) is not broken down properly.
A disturbance of consciousness marked by confusion, inattention, delusions, hallucinations, and agitation. It is distinguished from dementia by its relatively sudden onset and variation in the severity of symptoms.
A persistent false belief held in the face of strong contradictory evidence.
A group of symptoms (syndrome) associated with a chronic progressive impairment of memory, reasoning ability, and other intellectual functions, personality changes, deterioration in personal grooming, and disorientation.
False sensory perceptions; hearing sounds or seeing people or objects that are not there. Hallucinations can also affect the senses of smell, touch, and taste.
A part of the brain's limbic system that is involved in memory formation and learning.
Progressing gradually and inconspicuously, but with serious effects.
Magnetic resonance imaging (MRI)—
An imaging technique that uses electromagnetic radiation and a computer to obtain detailed images of soft tissues such as the brain.
Mild cognitive impairment (MCI)—
A transitional phase of memory loss in older people that precedes dementia or AD.
Neurofibrillary tangles—
Accumulations of twisted protein fragments inside nerve cells in the brain that are diagnostic of AD.
A nerve cell.
Chemicals that carry nerve impulses from one nerve cell to another. AD causes a drop in the production of several important neurotransmitters.
A neurotransmitter and adrenal hormone and the precursor of epinephrine.
Continuous involuntary repetition of speech or behavior.
A trait or disorder that is determined by several different genes. Most human characteristics, including height, weight, and general body build, are polygenic. Schizophrenia and late-onset AD are considered polygenic disorders.
A neurotransmitter found in the brain and blood. Low levels of serotonin are associated with AD.
  • What specific exercises will help AD patients?
  • What is the best type of exercise plan based on the AD symptoms?
  • How often and how long should physical exercises be performed?
  • How strenuous should an exercise routine be?
  • What exercises should not be done?
  • Will health insurance pay for physical therapy?
  • How can a good physical therapist be found to help patients with Alzheimer's disease?


AD cannot be prevented as long as the specific underlying causes remain unknown. However, early identification and treatment tend to slow the rate of progression. Exercise plays an important role in reducing the symptoms of AD. Physical therapy for AD patients is essential to help them maintain as normal a lifestyle as possible, retaining physical and mental functioning to the greatest degree possible. Exercise plans can be coordinated among various health care providers to meet the individual needs of each patient with AD.

See also Exercise ; Senior fitness .



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Consumer Dummies. Alzheimer's Disease for Dummies. Hoboken: John Wiley and Sons, 2016.

Sahyouni, Ronald, Aradhana Verma, and Jefferson Chen. Alzheimer's Disease Decoded: The History, Present, and Future of Alzheimer's Disease and Dementia. Hackensack: World Scientific, 2016.


Kumar, A., K. Narayanay, R. K. Chaudhary, et al. “Current Perspective of Stem Cell Therapy in Neurodegenerative and Metabolic Diseases.” Molecular Neurobiology. Published electronically November 4, 2016. doi: 10.1007/s12035-016-0217-4.

Lu, Y., R. Wang, Y. Dong, et al. “Low-Level Laser Therapy for Beta Amyloid Toxicity in Rat Hippocampus.” Neurobiology Again 49 (October 2016): 165–82.

Van der Schyf, Cornelis J. “Psychotropic Drug Development Strategies That Target Neuropsychiatric Etiologies in Alzheimer's and Parkinson's Diseases.” Drug Development Research. Published electronically November 4, 2016. doi: 10.1002/ddr.21368.

WEBSITES . “What Are the Seven Stages of Alzheimer's Disease?” (accessed November 7, 2016).

Fisher Center for Alzheimer's Research Foundation. “What Are the Goals of Alzheimer's Treatment?” (accessed November 7, 2016).

Mayo Clinic staff. “Alzheimer's Disease.” Mayo Clinic: Patient Care & Health Information, Diseaes & Conditions. Mayo . (accessed November 7, 2016).

MedlinePlus. “Alzheimer's Disease.” (accessed November 7, 2016).


Alzheimer's Association, 225 N. Michigan Avenue, Floor 17, Chicago, IL, 60601-7633, (312) 335-8700, Fax: (866) 335-5886, (800) 272-3900,, .

Alzheimer's Disease Education and Referral Center, National Institute on Aging, PO Box 8250, Silver Spring, MD, 20907, Fax: (301) 495-3334, (800) 438-4380,, .

Alzheimer's Foundation of America, 322 8th Avenue, 7th Floor, New York, NY, 10001, (866) 232-8484, .

Fisher Center for Alzheimer's Research Foundation, 110 East 42nd Street, New York, NY, 10017, (800) 259-4636,, .

Laith Farid Gulli, MD
Revised by David Edward Newton, EdD
Revised by William A. Atkins, BB, BS, MBA
Revised by L. Lee Culvert

  This information is not a tool for self-diagnosis or a substitute for professional care.