Alzheimer’s Disease

Alzheimer’s disease is a brain disorder that is a form of dementia, which is the loss of cognitive functioning—the ability to think, remember or reason—to such an extent that it interferes with a person's daily life and activities. These functions include memory, language skills, visual perception, problem solving, self-management and the ability to focus and pay attention. Some people with dementia cannot control their emotions, and their personalities may change. Several diseases and conditions can cause dementia or dementia-like symptoms, but dementia itself is not a specific disease.

In some dementias, changes in the tau protein, which plays an important role in the structure and formation of brain cells, cause it to form clumps inside nerve cells in the brain, which is believed to make the cells stop functioning properly and die. Disorders that are associated with the abnormal buildup of tau are called tauopathies.

In Alzheimer’s disease, the tau protein aggregates (accumulates into abnormal clumps) and becomes twisted and tangled, forming fibers—neurofibrillary or tau tangles—inside neurons. Abnormal clumps (plaques) of the beta-amyloid protein (a protein believed to play a role in the communication between brain cells) are prominent in spaces between brain cells. Both plaques and tangles are thought to contribute to reduced function and nerve-cell death in AD and are hallmarks of the disease.

There are two types of Alzheimer's—early-onset and late-onset. Both types have a genetic component. Most people with Alzheimer's have late-onset disease, in which symptoms become apparent in their mid-60s. 

Researchers have not found a specific gene that directly causes the late-onset form of the disease. However, one genetic risk factor—having one form, or allele, of the apolipoprotein E (APOE) gene on chromosome 19—does increase a person's risk. APOE ɛ4 is called a risk-factor gene because it increases a person's risk of developing the disease. However, inheriting an APOE ɛ4 allele does not mean that a person will definitely develop Alzheimer's. Some people with an APOE ɛ4 allele never get the disease, and others who develop Alzheimer's do not have any APOE ɛ4 alleles.

Signs of late-onset Alzheimer’s:

• Signs first appear in a person’s mid-60s
• Most common type of Alzheimer’s disease
• May involve a gene called APOE ɛ4

Early-onset Alzheimer's disease occurs between a person's 30s to mid-60s and represents less than 10 percent of all people with Alzheimer's. Some cases are caused by an inherited change in one of three genes. For other cases, research shows that other genetic components are involved. Researchers are working to identify additional genetic risk variants for early-onset Alzheimer's disease.

Signs of early-onset Alzheimer’s:

• Signs first appear between a person’s 30s and mid-60s
• Very rare
• Usually caused by gene changes passed down from parent to child

Age is the primary risk factor for developing dementia. For that reason, the number of people living with dementia could double in the next 40 years as the number of Americans aged 65 and older increases to more than 88 million in 2050. Regardless of the form of dementia, the personal, economic and societal demands can be devastating.

Various disorders and factors contribute to dementia, resulting in a progressive and irreversible loss of neurons and brain functions. Currently, there are no cures for these neurodegenerative disorders.

Alzheimer's disease is the most common cause of dementia in older adults. As many as five million Americans aged 65 and older may have the disease. In most neurodegenerative diseases, certain proteins abnormally clump together and are thought to damage healthy neurons, causing them to stop functioning and die. In Alzheimer's disease, fragments of a protein called amyloid form abnormal clusters called plaques between brain cells, and a protein called tau forms tangles inside nerve cells.

In 1906, Dr. Alois Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary, or tau, tangles).

These plaques and tangles in the brain are still considered some of the main features of Alzheimer’s disease. Another feature is the loss of connections between nerve cells (neurons) in the brain. Neurons transmit messages between different parts of the brain, and from the brain to muscles and organs in the body. Many other complex brain changes are thought to play a role in Alzheimer’s, too.

This damage initially takes place in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. It later affects areas in the cerebral cortex, such as those responsible for language, reasoning and social behavior. Eventually, many other areas of the brain are damaged.

It seems likely that damage to the brain starts a decade or more before memory and other cognitive problems appear. The damage often initially appears in the hippocampus, which is the part of the brain essential in forming memories. Ultimately, the plaques and tangles spread throughout the brain, and brain tissue shrinks significantly.

Researchers have not found a single gene solely responsible for Alzheimer's disease; rather, multiple genes are likely involved. One genetic risk factor—having one form of the apolipoprotein E (APOE) gene on chromosome 19—does increase a person's risk for developing Alzheimer’s. People who inherit one copy of this APOE ε4 allele have an increased chance of developing the disease; those who inherit two copies of the allele are at even greater risk. (An allele is a variant form of a pair of genes that are located on a particular chromosome and control the same trait.) The APOE ε4 allele may also be associated with an earlier onset of memory loss and other symptoms. Researchers have found that this allele is associated with an increased number of amyloid plaques in the brain tissue of affected people.

In frontotemporal disorders, changes to nerve cells in the brain's frontal lobes affect the ability to reason and make decisions, prioritize and multitask, act appropriately and control movement. Changes to the temporal lobes affect memory and how people understand words, recognize objects and recognize and respond to emotions. Some people decline rapidly over two to three years, while others show only minimal changes for many years. People can live with frontotemporal disorders for two to 10 years, sometimes longer. 

The following risk factors may increase a person's chance of developing one or more kinds of dementia. Some of these factors can be modified, while others cannot.

• Age: Advancing age is the best known risk factor for developing dementia.
• Hypertension: High blood pressure has been linked to cognitive decline, stroke and types of dementia that damage the white matter regions of the brain. High blood pressure causes “wear-and-tear” to brain blood vessel walls called arteriosclerosis.
• Stroke: A single major stroke or a series of smaller strokes increases a person's risk of developing vascular dementia. A person who has had a stroke is at an increased risk of having additional strokes, which further increases the risk of developing dementia.
• Alcohol: Most studies suggest that regularly drinking large amounts of alcohol increases the risk of dementia. Specific dementias are associated with alcohol abuse, such as Wernicke-Korsakoff syndrome.
• Atherosclerosis:The accumulation of fats and cholesterol in the lining of arteries, coupled with an inflammatory process that leads to a thickening of the vessel walls (atherosclerosis), can lead to stroke, which raises the risk for vascular dementia.
• Diabetes: People with diabetes appear to have a higher risk for dementia. Poorly controlled diabetes is a risk factor for stroke and cardiovascular disease, which in turn increases the risk for vascular dementia.
• Down syndrome: Many people with Down syndrome develop symptoms of Alzheimer's disease by the time they reach middle age.
• Genetics: The chance of developing a genetically linked form of dementia increases when more than one family member has the disorder. In many dementias, there can be a family history of a similar disease. In some cases, such as with frontotemporal degeneration (FTD), having just one parent who carries a mutation increases the risk of inheriting the condition. A very small proportion of dementia is inherited.   
• Head injury: An impact to the head can cause a traumatic brain injury (TBI). Certain types of TBI, or repeated TBIs, can cause dementia and other severe cognitive problems.
• Parkinson's disease: The degeneration and death of nerve cells in the brain in people with Parkinson's disease can cause dementia and significant memory loss.
• Smoking: Smoking increases the risk of developing cardiovascular diseases that slow or stop blood from getting to the brain.

The National Institute of Neurological Disorders and Stroke (NINDS) is a leading federal funder of research on nervous system disorders, including dementia. Another NIH institute, the National Institute on Aging (NIA), is a leading federal funder of research on Alzheimer's disease and Alzheimer's disease–related dementias. Although scientists have some understanding of the dementias and the mechanisms involved, ongoing research may lead to new ways to understand the cause(s) of the disease, diagnose, treat or perhaps prevent or block disease development.

Research partnerships on dementia involving NINDS and NIA include:

• The National Alzheimer's Project Act (NAPA), a coordinated national plan to address Alzheimer's disease and improve care and services. The project calls for increased collaboration among scientists, the federal government and public organizations while improving patient care. NAPA's National Plan to Address Alzheimer's Disease is designed to expand research in prevention and treatment of Alzheimer's disease and related dementias, and to move the most promising drugs from discovery into clinical trials. The plan also calls for increased federal funding for AD research, as well as support for those affected by AD and their families, increased public awareness about AD, and improved data collection and analysis. These goals also apply to dementia with Lewy bodies as well as frontotemporal, mixed and vascular dementias. The plan's overarching research goal is to “prevent or effectively treat Alzheimer's disease by 2025.”
• The Accelerating Medicines Partnership® Program for Alzheimer's Disease (AMP® AD), a multi-sector partnership among the NIH, 10 biopharmaceutical companies and several nonprofit organizations to develop new clinically relevant therapeutics and biomarkers to confirm existing therapies. The goal is to speed up the process of bringing new medicines to people with AD or who are at risk for developing AD.
• M2OVE—AD: Molecular Mechanisms of the Vascular Etiology of Alzheimer's Disease, a program that allows scientists from diverse fields to work collaboratively to understand the complex molecular mechanisms by which vascular risk factors influence AD. The work also identifies new targets for treatment and prevention. It builds on the open-science approach and the big data infrastructure established by the AMP® AD mentioned above.
• The Tau Center Without Walls program, designed to increase collaboration and sharing of data and resources among researchers to better understand the protein tau and its involvement in such disorders as frontotemporal degeneration (FTD). These efforts may lead to advances in prevention, diagnosis or treatment of tau toxicity associated with FTD, and contribute to tool development that can be applied in FTD clinical trials and other tau-related disorders.
• The Dementia with Lewy Body Biomarkers Consortium, designed to expand the collection of clinical data and biological specimens in NINDS’s Parkinson's Disease Biomarkers Program to include data from people with Lewy body dementias. Standardized research and data collection and reporting systems will make it easier for researchers to share and confirm their research.
• The Small Vessel Vascular Contributions to Cognitive Impairment and Dementia (VCID) Biomarkers Program. Researchers in this program hope to develop biomarkers of key vascular processes related to VCID in Alzheimer's disease. Identifying biomarkers may improve the efficiency and outcome of trials designed to test drug effectiveness and safety in humans, and speed the development of therapies for the dementias.

NINDS and NIA are sponsoring additional research on age-related and other dementias:

• Clinical studies offer an opportunity for helping researchers find better ways to safely detect, treat or prevent dementias. Various NIH institutes support clinical studies on AD and related dementias at the NIH research campus in Bethesda, Maryland, and at medical research centers across the U.S.
  • For information about participating in clinical studies, visit NIH Clinical Research Trials and You.
  • For a list of clinical trials and studies for AD and related dementias, visit Alzheimers.gov.
  • For a comprehensive list of all clinical trials, visit Clinicaltrials.gov and type in the name of the dementia (e.g., “Lewy body dementia” or “vascular dementia”).
• Several research projects hope to identify biomarkers (measurable biological signs that may indicate disease risk and progression or confirm diagnosis) for the dementias. Such biomarkers could be detected through imaging or even blood tests. Research projects include the study of possible biomarkers to predict cognitive decline in people with Parkinson's disease, the Alzheimer's Biomarkers Consortium in Down Syndrome (many people with Down syndrome have Alzheimer's-related brain changes in their 30s that can lead to dementia in their 50s and 60s), and genetic and biomarker studies that may lead to promising treatments for FTD. The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a longitudinal study to validate the use of biomarkers for Alzheimer's disease clinical trials and diagnosis.
• A number of drugs and compounds that might slow the progression of AD and other dementias are in various stages of testing. A NINDS study found that tau antisense oligonucleotides—compounds that are genetically engineered to block a cell's assembly-line production of the toxic form of the tau protein—could prevent and reverse some of the brain injury in animal models of the disease. NIH-supported prevention trials are testing drugs that target amyloid proteins that form plaques in the brain. Other NIH studies include the use of drugs being developed to treat autism spectrum disorders to see if they can improve cognitive functions in people with age-related cognitive decline.
• Physical activity can benefit mental well-being and improve daily functioning and quality of life in people with dementia. Researchers are assessing the combined approach of aerobic and cognitive exercise to see if it can delay or slow the progression of Alzheimer's disease in at-risk older adults. Other research is assessing the benefit of exercise to delay mild cognitive impairment in older individuals, and to improve brain function in older adults who may be at risk for developing AD.
• NIH scientists continue to look for new genes that may be responsible for the development of AD and other forms of dementia. One approach is using genome-wide association studies, which can rapidly scan the complete sets of DNA, or genomes, of many people to find genetic variations associated with a particular disease. The NIH hopes to identify new genetic associations for neurodegenerative diseases that may lead to better strategies to detect, treat and prevent dementias.
• Clinical imaging may help researchers better understand changes in the brains of people with dementia, as well as help diagnose these disorders. For example, researchers hope to enhance brain imaging techniques to make it possible to detect, and therefore try to stop, the earliest changes in the protective blood-brain barrier that may contribute to vascular contributions to cognitive impairment and dementia. 
• The International Alzheimer's Disease Research Portfolio (IADRP) helps individuals learn about research related to AD dementias at both public and private organizations around the world. It also helps organizations leverage resources to avoid duplication of efforts. The Common Alzheimer's Disease Research Ontology—a classification system that allows organizations to integrate and compare research portfolios—was developed by the NIA, NIH and Alzheimer's Association.
• Studying groups of people over time may lead to ways to identify those at risk of developing dementia or cognitive impairment. Three NIH-funded research teams are conducting longitudinal studies of individuals in which frontotemporal disorders run in families and appear on their own (sporadic) to understand the progression of FTD both before and after symptom onset; identify genes; discover biomarkers for diagnosis, progression and prognosis; and establish a clinical research consortium to support FTD therapy development.
• A number of proteins—including tau, alpha-synuclein, TDP-43 and amyloid-beta—are involved with various cellular processes. When there is a change in the genes that direct the production or rate of clearance (degradation) of these proteins, the proteins can build up in unusual amounts and form abnormal clumps that damage nerve cells in the brain, causing dementia and other symptoms such as motor function disorders. NIH-funded research projects are aimed at better understanding the toxic effects of protein buildup and how it is related to the development of dementia. A number of studies are targeting the buildup of amyloid, which forms plaques that are characteristic in Alzheimer's disease. Other research hopes to better understand how proteins become harmful in frontotemporal disorders and Lewy body dementia.
• Stem cells are unique in that they have the potential to develop into many different cell types in the body, including brain cells. Scientists are exploring them to discover nerve cell mechanisms that lead to the onset and progression of AD and other forms of dementia. For example, scientists converted human skin cells into a model of human neurons. Such neurons, when created from individuals with familial forms of AD, show biochemical changes that represent the disease. Researchers are investigating the mechanism by which human AD neurons develop cellular and molecular defects in protein production and degradation.

The signs and symptoms of dementia and Alzheimer’s disease may vary greatly among individuals as different parts of the brain are affected. 

Doctors have identified a range of conditions that can cause dementia or dementia-like symptoms. The diseases have different symptoms that involve body and brain functions, and affect mental health and cognition. For example, as Alzheimer's disease progresses, people experience greater memory loss and other cognitive difficulties. Problems can include wandering and getting lost, trouble handling money and paying bills, repeating questions, taking longer to complete daily tasks, and personality and behavior changes.

People are often diagnosed as a combination of these symptoms are observed. Memory loss and confusion worsen, and people begin to have problems recognizing family and friends. They may be unable to learn new things, carry out multi-step tasks such as getting dressed, or cope with new situations. In addition, people at this stage may have hallucinations, delusions and paranoia and may behave impulsively.

People with severe Alzheimer's disease cannot communicate and are completely dependent on others for their care. The person may be in bed most or all of the time as body functions shut down. Certain drugs can temporarily slow some symptoms of Alzheimer's from getting worse, but currently there are no treatments that stop the progression of the disease. 

Overall, symptoms of dementia are different depending on the cause. If you are experiencing or witnessing any combination of the following cognitive, psychological and behavioral changes, it may be time to see a doctor:

• Depression, anxiety and agitation
• Paranoia
• Personality changes or unusual/inappropriate behavior
• Hallucinations
• Disorientation and confusion in normal situations
• Notable memory loss
• Struggling to find the right words/communication problems
• Complex tasks have become more difficult
• Struggling with basic gross- and fine-motor function
• Coordination issues
• Disorientated while planning, organizing or navigating (e.g., driving a well-known route)

To diagnose dementia and Alzheimer’s disease, doctors will first assess whether an individual has an underlying treatable condition such as abnormal thyroid function, vitamin deficiency or normal pressure hydrocephalus that may relate to cognitive difficulties. Additionally, reviewing all prescribed medications and their contraindications may be an easy diagnosis. 

Early detection of symptoms is important, as some causes can be treated. In many cases, the specific type of dementia may not be confirmed until after the person has died and the brain is examined.

An assessment may include:

• Medical history and physical exam: Assessing a person's medical and family history, current symptoms and medication, and vital signs can help the doctor detect conditions that might cause or occur with dementia. Some conditions may be treatable.
• Neurological evaluations: Examining balance, sensory response, reflexes and other functions can help doctors identify signs of conditions that may affect the diagnosis or are treatable with drugs. Doctors also might use an electroencephalogram (EEG), a test that records patterns of electrical activity in the brain, to check for abnormal electrical brain activity.
• Brain scans: Computed tomography (CT) and magnetic resonance imaging (MRI) can detect structural abnormalities and rule out other causes of dementia. Positron-emission tomography (PET) can look for patterns of altered brain activity that are common in dementia. Advances in PET can detect amyloid plaques and tau tangles in AD.
• Cognitive and neuropsychological tests: These tests are used to assess memory, language skills, math skills, problem-solving and other abilities related to mental functioning.
• Laboratory tests: Testing a person's blood and other fluids, as well as checking levels of various chemicals, hormones and vitamin levels, can identify or rule out conditions that may contribute to dementia.
• Presymptomatic tests: Genetic testing can help some people who have a strong family history of dementia identify their own risks.
• Psychiatric evaluation: This evaluation can help determine if depression or another mental health condition is causing or contributing to a person's symptoms.

Additionally, biomarker tests are used in studies to measure biological changes in the brain associated with Alzheimer's disease and criteria for documenting and reporting Alzheimer's-related changes observed during an autopsy.

Treating the symptoms of Alzheimer’s can help provide people with comfort, dignity and independence for a longer period of time and also assist their caregivers. Galantamine, rivastigmine and donepezil are cholinesterase inhibitors that are prescribed for mild to moderate Alzheimer’s symptoms. These drugs may help reduce or control some cognitive and behavioral symptoms.

Cholinesterase inhibitors prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking. As Alzheimer’s progresses, the brain produces less acetylcholine and, over time, these medicines eventually lose their effectiveness. Because cholinesterase inhibitors work in a similar way, switching from one to another may not produce significantly different results, but a person living with Alzheimer’s may respond better to one drug versus another.

Lecanemab and aducanumab are immunotherapies with FDA Accelerated Approval to treat early Alzheimer’s. These drugs target the protein beta-amyloid to help reduce amyloid plaques, one of the hallmark brain changes in Alzheimer’s. Clinical studies to determine the effectiveness of lecanemab and aducanumab were conducted only in people with early-stage Alzheimer’s, or mild cognitive impairment due to the disease. Study results showed lecanemab slowed the rate of cognitive decline among study participants over the course of 18 months and reduced the levels of amyloid in the brain. Study results for aducanumab showed a reduction in amyloid buildup in the brain, as well, but uncertainty in the drug’s ability to slow cognitive decline. Further research is in progress to test these drugs’ ability to slow cognitive decline.

To gain full FDA approval, the drug companies must conduct additional studies on the clinical benefits of the medications. Currently, insurance may only cover these medications in specific situations.

Before prescribing these medications, doctors may order PET scans or an analysis of cerebrospinal fluid to evaluate whether amyloid deposits are present in the brain. There are possible side effects to taking these medications, including amyloid-related imaging abnormalities (ARIA), which can lead to fluid buildup or bleeding in the brain. ARIA symptoms are generally mild, but in rare instances they may be serious and life-threatening. Due to this potential risk, monitoring with routine MRIs for side effects related to ARIA is required.

Several other disease-modifying medications are being tested in people with mild cognitive impairment or early Alzheimer’s.

A medication known as memantine, an N-methyl-D-aspartate (NMDA) antagonist, can be prescribed to treat moderate to severe Alzheimer’s. This drug’s main effect is to decrease symptoms, which could enable some people to maintain certain daily functions a little longer than they would without the medication. For example, memantine may help a person in the later stages of the disease maintain their ability to use the bathroom independently for several more months, a benefit for both people with Alzheimer’s and their caregivers.

Memantine is believed to work by regulating glutamate, an important brain chemical. When produced in excessive amounts, glutamate may lead to brain cell death. Because NMDA antagonists work differently from cholinesterase inhibitors, the two types of drugs can be prescribed in combination.

The FDA has also approved donepezil, the rivastigmine patch and a combination medication of memantine and donepezil for the treatment of moderate to severe Alzheimer’s.

Doctors usually start patients at low drug doses and gradually increase the dosage based on how well a patient tolerates the drug. There is some evidence that certain people may benefit from higher doses of Alzheimer’s medications. However, the higher the dose, the more likely unwanted side effects will occur.

Patients should be monitored when a drug is started. All of these medicines have possible side effects that may include nausea, vomiting, diarrhea, allergic reactions, loss of appetite, headaches, confusion, dizziness and falls. Report any unusual symptoms to the prescribing doctor right away.

It is important to follow the doctor’s instructions when taking any medication, including vitamins and herbal supplements. Talk with your doctor before adding or changing any medications.

The following list provides an overview of Alzheimer’s medications. It’s important to talk with your healthcare provider about your treatment options and which ones may be most appropriate for you.

• Donepezil. Cholinesterase inhibitor. Treats mild, moderate and severe Alzheimer’s by preventing the breakdown of acetylcholine in the brain. Possible side effects include nausea, vomiting, diarrhea, insomnia, muscle cramps, fatigue and weight loss. Delivered orally once a day through a tablet that is either swallowed or dissolves in the mouth.
• Rivastigmine. Cholinesterase inhibitor. Treats mild, moderate and severe Alzheimer’s by preventing the breakdown of acetylcholine and butyrylcholine (a chemical similar to acetylcholine) in the brain. Possible side effects include nausea, vomiting, diarrhea, weight loss, indigestion, decreased appetite, anorexia and muscle weakness. Delivered orally through a capsule twice a day or through a skin patch that is replaced once a day.
• Galantamine. Cholinesterase inhibitor. Treats mild to moderate Alzheimer’s by preventing the breakdown of acetylcholine and stimulates nicotinic receptors to release more acetylcholine in the brain. Possible side effects include nausea, vomiting, diarrhea, decreased appetite, weight loss, dizziness and headache. Delivered orally through an extended-release capsule, tablet or liquid. Extended-release capsule is taken once a day. Tablet and oral solution are each taken twice a day.
• Memantine. NMDA antagonist. Treats moderate to severe Alzheimer’s by blocking the toxic effects associated with excess glutamate and regulates glutamate activation. Possible side effects include dizziness, headache, diarrhea, constipation and confusion. Delivered orally through an extended-release capsule, tablet or liquid. Extended-release capsule is taken once a day. Tablet and oral solutions are each taken once a day.
• Memantine and Donepezil (manufactured combination). NMDA antagonist. Treats moderate to severe Alzheimer’s by blocking the toxic effects associated with excess glutamate and prevents the breakdown of acetylcholine in the brain. Possible side effects include headache, nausea, vomiting, diarrhea, dizziness, anorexia and ecchymosis (small bruising from leaking blood vessels). Delivered orally through an extended-release capsule once a day.

• Aducanumab. Disease-modifying immunotherapy. Treats mild cognitive impairment or mild Alzheimer’s by removing abnormal beta-amyloid to help reduce the number of plaques in the brain. Possible side effects include ARIA, headache, dizziness, falls, diarrhea and confusion. Delivered through IV over one hour every four weeks.
• Lecanemab. Disease-modifying immunotherapy. Treats mild cognitive impairment or mild Alzheimer’s by removing abnormal beta-amyloid to help reduce the number of plaques in the brain. Possible side effects include ARIA, headache, cough, diarrhea, nausea, vomiting, fever, chills, body aches, fatigue, high blood pressure, low blood pressure and low oxygen. Delivered through IV over one hour every two weeks.

With recovery and treatment of all dementia diagnoses, a team of specialists—doctors, nurses and speech, physical and other therapists—familiar with these disorders can help guide patients and their loved ones with care.

A dementia care team may involve neurologists, neuroscientists, psychiatrists and psychologists who will collaborate in order to determine the most appropriate treatment for your individualized diagnosis.  

There are also therapeutic modalities that may help with memory and cognitive processes, as well as contribute to an improvement in overall emotional wellness. 

Reminiscence therapy sessions can be organized in group format or conducted one on one. This method includes using discussions and memory triggers to help patients reform their memories. Tools like music, souvenirs or treasures from important places and moments in their life are used in this approach.

Cognitive stimulation therapy (CST) is group therapy that stimulates various parts of the brain through activities like word games, cooking, discussing current events and music. 

Some dementia patients may benefit from reality orientation training, which involves actions like hanging signs around the home to identify objects and memories or repeating the person’s name, today’s date and the time of day. Additionally, removing clutter from the home and limiting peripheral noises and sensory stimulating appliances like TVs and radios can help those with dementia stay focused. It’s also important to remove or relocate anything dangerous from the home, such as firearms or knives, and to hide car keys.     

Lifestyle changes, daily routines and structure also help patients with their morale, as well as overall physical health. Fitness classes or walks for cardiovascular health are always beneficial, as are light activities and pastimes like gardening, dancing or household chores. A diet rich in foods that are good for the brain and healthy sleep habits also contribute to overall wellness. 

Working with specialists and occupational and physical therapists can help with maintaining physical movement, address speech and swallowing issues, and help people learn new ways to handle loss of skills with everyday tasks such as feeding oneself. It is important to educate family, friends and caregivers about a loved one's medical issues. Also, in-person and online support groups available through many disease awareness and caregiver advocacy organizations can give families and other caregivers additional resources, as well as opportunities to share experiences and express concerns.

People living with Alzheimer’s and their caregivers must watch closely for side effects from these medications.

• Sleep aids are used to help people get to sleep and stay asleep. People with Alzheimer’s should not use these drugs regularly because they make the person more confused and more likely to fall. There are lifestyle changes people can make to improve their sleep. Learn more about getting a good night’s sleep.
• Anti-anxiety drugs are used to treat agitation. Certain types of anti-anxiety drugs, like benzodiazepines, can cause sleepiness, dizziness, falls and confusion. For this reason, doctors recommend they only be used for short periods of time, if at all.
• Anticonvulsants are drugs sometimes used to treat severe aggression. Side effects may cause sleepiness, dizziness, mood swings and confusion.
• Antipsychotics are drugs used to treat hallucinations, delusions, paranoia, agitation and aggression. Side effects of using these drugs can be serious, including increased risk of death in some older people with dementia. They should only be given to people with Alzheimer’s when the doctor agrees the symptoms are severe.

Alzheimer’s researchers continue to explore a variety of innovative approaches to treat symptoms as well as underlying disease processes. In ongoing clinical trials, they are developing and testing several new possible interventions. These include additional immunotherapy and other drug therapies, cognitive training, diet and physical activity.