Dementia

The different forms of age-related dementia, as well as many age-related neurodegenerative diseases, are thought to be caused by changes in various proteins. These diseases are called proteinopathies because they involve the abnormal buildup of specific proteins in the brain. Mutations in genes that provide instructions for making these proteins have been found to cause dementia in families. 

In the vast majority of affected individuals, dementia is not inherited, and the cause is unknown. 

Various neurodegenerative disorders and factors contribute to the development of dementia through a progressive and irreversible loss of neurons and brain functioning. Types of dementia include:

• Alzheimer’s disease, the most common dementia diagnosis among older adults. It is caused by changes in the brain, including abnormal buildups of proteins known as amyloid plaques and tau tangles.
• Frontotemporal dementia, a rare form of dementia that tends to occur in people younger than 60. It is associated with abnormal amounts or forms of the proteins tau and TDP-43.
• Lewy body dementia, a form of dementia caused by abnormal deposits of the protein alpha-synuclein, called Lewy bodies
• Vascular dementia, a form of dementia caused by conditions that damage blood vessels in the brain or interrupt the flow of blood and oxygen to the brain
• Mixed dementia, a combination of two or more types of dementia. For example, through autopsy studies involving older adults who had dementia, researchers have identified that many people had a combination of brain changes associated with different forms of dementia.

Doctors have identified many other 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.

Argyrophilic grain disease is a common, late-onset degenerative disease that affects brain regions involved in memory and emotion. It causes cognitive decline and changes in memory and behavior, with difficulty finding words. The disease’s signs and symptoms are indistinguishable from late-onset AD. Confirmation of the diagnosis can be made only at autopsy. 

Creutzfeldt-Jakob disease (CJD) is a rare brain disorder characterized by rapidly progressing dementia. Scientists have found that infectious proteins called prions become misshapen and tend to clump together, which causes brain damage. Initial symptoms include impaired memory, judgment and thinking, along with loss of muscle coordination and impaired vision. Some symptoms of CJD can be similar to symptoms of other progressive neurological disorders, such as Alzheimer’s disease.

Chronic traumatic encephalopathy (CTE) is caused by repeated traumatic brain injury (TBI) in some people with multiple concussions. People with CTE may develop dementia, poor coordination, slurred speech and other symptoms similar to those seen in Parkinson’s disease 20 years or more after the injury. Late-stage CTE is also characterized by brain atrophy and widespread deposits of tau in nerve cells. In some people, even just five to 10 years beyond the traumatic brain injury, behavioral and mood changes may occur. Dementia may not yet be present and the brain may not have started to shrink, but small deposits of tau are seen in specific brain regions at autopsy.

Huntington’s disease is an inherited, progressive brain disease that affects a person’s judgment, memory and ability to plan and organize, along with other cognitive functions. Symptoms typically begin around age 30 to 40 years and include abnormal and uncontrollable movements (chorea) as well as problems with walking and lack of coordination. Cognitive problems worsen as the disease progresses, and problems controlling movement lead to complete loss of ability for self-care.

HIV-associated dementia (HAD) can occur in people with human immunodeficiency virus, the virus that causes AIDS. HAD damages the brain’s white matter and leads to a type of dementia associated with memory problems, social withdrawal and trouble concentrating. People with HAD may develop movement problems as well. The incidence of HAD has dropped dramatically with the availability of effective antiviral therapies for managing the underlying HIV infections.

Vascular contributions to cognitive impairment and dementia (VCID) cause significant changes to memory, thinking and behavior. Cognition and brain function can be significantly affected by the size, location and number of brain injuries. Vascular dementia and vascular cognitive impairment arise as a result of risk factors that similarly increase the risk for cerebrovascular disease (stroke), including atrial fibrillation, hypertension, diabetes and high cholesterol. Symptoms of VCID can begin suddenly and progress or subside during one’s lifetime. VCID can occur along with Alzheimer’s disease. People with VCID almost always have abnormalities in the brain on magnetic resonance imaging (MRI) scans. These include evidence of prior strokes, often small and asymptomatic, as well as scattered changes in the brain’s “white matter," or the connecting “wires” of the brain that are critical for relaying messages between brain regions. Microscopic brain examination shows thickening of blood vessel walls called arteriosclerosis and thinning or loss of components of the white matter.

Forms of VCID include:

• Vascular dementia, which refers to progressive loss of memory and other cognitive functions caused by vascular injury or disease within the brain. Symptoms of vascular dementia may sometimes be difficult to distinguish from Alzheimer’s disease. Problems with organization, attention, slowed thinking and problem solving are all more prominent in VCID, while memory loss is more prominent in Alzheimer’s.
• Vascular cognitive impairment, which involves changes with language, attention and the ability to think, reason and remember that are noticeable but are not significant enough to greatly affect daily life. These changes, caused by vascular injury or disease within the brain, progress slowly over time.
• Post-stroke dementia, which can develop months after a major stroke. Not everyone who has had a major stroke will develop vascular dementia, but the risk for dementia is significantly higher in someone who has had a stroke.
• Multi-infarct dementia, which is the result of many small strokes (infarcts) and ministrokes. Language or other functions may be impaired, depending on the region of the brain that is affected. The risk for dementia is significantly higher in someone who has had a stroke. Dementia is more likely when strokes affect both sides of the brain. Even strokes that don’t show any noticeable symptoms can increase the risk of dementia.
• Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an extremely rare, inherited disorder caused by a thickening of the walls of small and medium-sized blood vessels, which reduces the flow of blood to the brain. CADASIL is associated with multi-infarct dementia, stroke and other disorders. The first symptoms can appear in people between ages 20 and 40. CADASIL may have symptoms that can be confused with multiple sclerosis. Many people with CADASIL are undiagnosed.
• Subcortical vascular dementia (previously known as Binswanger’s disease) involves extensive microscopic damage to the small blood vessels and nerve fibers that make up white matter, tissue that transmits signals between different areas of the brain, as well as between the brain and other parts of the body. Some consider it an aggressive form of multi-infarct dementia. Cognitive changes include problems with short-term memory, organization, attention, decision making and behavior. Symptoms tend to begin after age 60, and they progress in a stepwise manner. People with subcortical vascular disease often have high blood pressure, a history of stroke, or evidence of disease of the large blood vessels in the neck or heart valves.
• Cerebral amyloid angiopathy is a buildup of amyloid plaques in the walls of blood vessels in the brain. It is generally diagnosed when multiple tiny bleeds in the brain are discovered using MRI.

Reversible dementia-like disorders and conditions:

• Normal pressure hydrocephalus is a buildup of cerebrospinal fluid in the brain. Elderly individuals with the condition usually have trouble walking and with bladder control before the onset of dementia. 
• Nutritional deficiencies of vitamin B1 (thiamine), caused by chronic alcoholism, and of vitamin B12 can be reversed with treatment. 
• Side effects of medications or drug combinations may cause cognitive impairment that resembles degenerative or vascular dementia.
• Vasculitis, an inflammation of brain blood vessels, can cause dementia after multiple strokes.
• Subdural hematoma, or bleeding between the brain’s surface and its outer covering (the dura), is common after a fall. Subdural hematomas can cause dementia-like symptoms and changes in mental function. 
• Some non-malignant brain tumors can cause symptoms resembling dementia; recovery occurs following their removal by neurosurgery.
• Some chronic infections around the brain, so-called chronic meningitis, can cause dementia.

Dementia is the result of changes in certain brain regions that cause neurons (nerve cells) and their connections to stop working properly. Researchers have connected changes in the brain to certain forms of dementia and are investigating why these changes happen in some people but not others. For a small number of people, rare genetic variants that cause dementia have been identified.

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.

Multi-infarct dementia (MID) is a common cause of memory loss in older people. MID is caused by multiple strokes (disruption of blood flow to the brain) that lead to damaged brain tissue. Some strokes may occur without noticeable symptoms; doctors may refer to these as “silent strokes.”

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.

In other dementias and some brain disorders, the protein synuclein (believed to play an integral role in regulating the release of neurotransmitters) becomes misshapen and forms harmful clumps inside neurons in different brain regions. Disorders in which synuclein builds up inside neurons are called synucleinopathies. Changes in synuclein and/or its function are the basis of Lewy body dementia (LBD) and other disorders, such as multiple system atrophy. 

Multiple system atrophy is a progressive neurodegenerative disorder characterized by a combination of symptoms that affect both the autonomic nervous system (the part of the nervous system that controls involuntary action such as blood pressure or digestion) and movement. These changes cause parkinsonism, a condition resembling Parkinson’s disease.

Some specific causes of dementia disorders are explained below.

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.

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 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. 

Lewy body dementia includes two related conditions—dementia with Lewy bodies and Parkinson’s disease dementia. In dementia with Lewy bodies, the cognitive symptoms are seen within a year of movement symptoms called parkinsonism (including tremor, difficulty with walking and posture, and rigid muscles). In Parkinson’s disease dementia, the cognitive symptoms develop more than a year after movement problems begin.

1. Dementia with Lewy bodies (DLB) is one of the more common forms of progressive dementia. Symptoms such as difficulty sleeping, loss of smell, and visual hallucinations often precede movement and other problems by as many as 10 years. Later in the course of DLB, some signs and symptoms are similar to Alzheimer’s disease and may include memory loss, poor judgment and confusion. Other signs and symptoms of DLB are similar to those of Parkinson’s disease, including difficulty with movement and posture, a shuffling walk and changes in alertness and attention. There is no cure for DLB, but there are drugs that control some symptoms.
2. Parkinson’s disease dementia (PDD) can occur in people with Parkinson’s disease, but not all people with Parkinson’s disease will develop dementia. PDD may affect memory, social judgment, language or reasoning. The time from the onset of movement symptoms to the onset of dementia symptoms varies greatly from person to person. Risk factors for developing PDD include the onset of Parkinson’s-related movement symptoms followed by mild cognitive impairment and REM sleep behavior disorder, which involves having frequent nightmares and hallucinations.

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, 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.

There are currently no treatments to stop or slow dementia in neurodegenerative diseases. Some diseases that occur at the same time as dementia, such as diabetes and depression, can be treated. Other symptoms that may occur in dementia-like conditions can also be treated, although some symptoms may only respond to treatment for a period of time. Medications are available to treat certain behavioral symptoms, as well as delusions, depression, muscle stiffness and risk factors for vascular cognitive impairment such as high blood pressure. Always consult with a doctor, as some medications may make symptoms worse.

Most drugs for dementia are used to treat symptoms in AD. One class of drugs, cholinesterase inhibitors, can temporarily improve or stabilize memory and thinking skills in some people by increasing the activity of the cholinergic brain network—a subsystem in the brain that is highly involved with memory and learning. These drugs include donepezil, rivastigmine and galantamine.

The drug memantine is in another class of medications called NMDA receptor antagonists, which prevent declines in learning and memory. Memantine may be combined with a cholinesterase inhibitor for added benefits. The U.S. Food and Drug Administration (FDA) approved the drug aducanumab (Aduhelm™) to reduce the buildup of harmful amyloid beta plaques.

There are no medications approved to treat or prevent frontotemporal disorders and most other types of progressive dementia. Sedatives, antidepressants and other drugs used to treat Parkinson’s and Alzheimer’s symptoms may help manage certain symptoms and behavioral problems associated with the disorders.

Medicines available for managing Lewy body dementia are aimed at relieving symptoms such as gait and balance disturbances, stiffness, hallucinations and delusions. Studies suggest that the cholinesterase inhibitor drugs for Alzheimer’s disease may offer some benefit.

Some studies suggest that the cholinesterase inhibitors used to treat people with AD might improve cognitive, behavioral and psychotic symptoms in people with Parkinson’s disease dementia. Many of the medications used to treat the motor symptoms of PD worsen the cognitive problems. The FDA has approved rivastigmine (an Alzheimer’s drug) to treat cognitive symptoms in PDD.

Vascular dementia is often managed with drugs that prevent strokes or reduce the risk of additional brain damage. Some studies suggest that drugs that improve memory in AD might benefit people with early vascular dementia. Treating the modifiable risk factors can help prevent additional strokes.

In cases of reversible dementia-like disorders, many conditions that cause symptoms can be halted or even reversed with the appropriate treatment.

Normal pressure hydrocephalus: This buildup of cerebrospinal fluid in the brain can be treated or even reversed by implanting a shunt system to divert fluid from the brain.

Nutritional deficiencies of vitamin B1 (thiamine) can be reversed with treatment. People who have abused substances such as alcohol and recreational drugs sometimes display signs of dementia even after the substance abuse has stopped.

• Side effects of medications or drug combinations can reverse upon stopping these medications. 
• Vasculitis is an inflammation of brain blood vessels and may be treated with immunosuppressive medications.
• Subdural hematoma, or bleeding between the brain’s surface and its outer covering (the dura), is common after a fall. With treatment, some symptoms can be reversed.
• Recovery for non-malignant brain tumors occurs following their removal by neurosurgery.
• Chronic meningitis may be treatable by drugs that kill the infectious agent.

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.