Disease Resources

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The latest disease information compiled by our experts.

What is Alzheimer’s disease?

Alzheimer’s disease (AD) is a brain disorder that slowly impairs memory and thinking skills. AD is the most common cause of dementia, which leads to a decline in thinking that interferes with one’s everyday functions. An estimated 7 million Americans over the age of 65 have AD, and it is the seventh leading cause of death in the U.S.

What are the causes of Alzheimer’s disease?

In most cases, the cause of AD is unknown. In AD, the brain contains abnormal protein deposits called plaques (made up of amyloid protein) and tangles (composed of tau protein). These deposits begin 10-20 years before a person develops symptoms of the disease. In rare cases, AD is caused by a genetic mutation that leads to excess amyloid protein in the brain. Scientists have learned a great deal about what factors may increase a person’s risk of developing AD. 

The single most important risk factor for developing AD is age. The likelihood of developing AD doubles every 5 years after age 65.

Additional factors that appear to increase the risk of developing AD include:

  • Family history of AD
  • Other health conditions, such as diabetes and high blood pressure
  • Lack of physical activity
  • Obesity and/or a poor diet
  • Smoking
  • Limited education

What are the symptoms of Alzheimer’s disease?

AD is often described in “stages.” Each stage has typical symptoms, though these may vary from person to person. Progression from one stage to the next is gradual.

Early stage (mild)

AD begins gradually and may, at first, be difficult to recognize. People are often diagnosed in this stage.

Common early symptoms include:

  • Forgetting recent events and conversations
  • Repeating questions
  • Misplacing things
  • Having trouble finding one’s way around and getting lost
  • Taking longer to complete normal daily tasks
  • Having difficulty completing complex tasks, such as paying bills
  • Struggling to find the rights words to express thoughts

Middle stage (moderate)

Memory loss and confusion progress and people find it more difficult to:

  • Remember information from their past
  • Know their surroundings (which can lead to wandering)
  • Recognize family and friends
  • Choose proper clothing and get dressed
  • Language: read, write, and speak

Late stage (severe)

A person with advanced AD is often unable to: 

They may sleep much of the time and usually need full-time care.

  • Communicate
  • Recognize people, places, or objects
  • Walk

They may sleep much of the time and usually need full-time care.

Other symptoms

Other symptoms that can occur at any stage include changes in:

  • Mood, such as irritability, anxiety, or depression
  • Personality, such as becoming withdrawn or impulsive
  • Behavior, including agitation
  • Thought processes, such as believing things are happening that are not true, or seeing/hearing things that are not there

How is Alzheimer’s disease diagnosed?

No single test leads to a diagnosis of AD. Rather a diagnosis is made after a complete evaluation that includes:

  • A detailed history and physical exam, including information from family or others who know the person well
  • Tests to evaluate memory and thinking
  • Blood tests, brain scans, and in some cases genetic tests or spinal fluid testing

There are now blood tests and brain scans that can detect the changes of Alzheimer’s disease, but it is important for doctors to also look for other conditions that could impair memory and have a different treatment.

What are the prognosis and treatment options?

There is no known cure for AD. The duration of the disease can vary from a few years to more than 20, though most people live 8-10 years after being diagnosed. There are several prescription drugs used to slow the symptoms and progression of AD:

Medications (pills or skin patches) that treat the chemical changes that occur in the brain:

  • Donepezil (Aricept®)
  • Galantamine (Razadyne®)
  • Benzgalantamine (Zunveyl®)
  • Rivastigmine (Exelon®)
  • Memantine (Namenda®)
  • A drug containing both donepezil and memantine, called Namzaric®

Medications (intravenous—given through a vein) that remove the amyloid plaque build-up that occurs in the brain:

  • Lecanemab (Leqembi®)
  • Donanemab (Kisunla®)

Where can I learn more?

More information about Alzheimer's disease can be found at:

What is frontotemporal dementia?

Frontotemporal dementia (FTD) refers to a group of diseases that damage the frontal and temporal lobes of the brain, resulting in significant changes in behavior, language, and/or motor function.

FTD types can be differentiated by the areas impacted: 

  • Behavior
    • Behavioral variant frontotemporal dementia
  • Language
    • Primary progressive aphasia (PPA), of which there are 3 types:
      • Semantic PPA
      • Nonfluent/agrammatic PPA
      • Logopenic PPA
  • Motor Function (with or without behavior or language problems)
    • Amyotrophic lateral sclerosis (ALS)
    • Corticobasal syndrome (CBS)
    • Progressive supranuclear palsy (PSP)

FTD accounts for only about 5% of all dementia cases in the United States but is one of the most common types of dementia in younger individuals. Approximately 60% of people with FTD are 45 to 64 years old.

What are the causes of frontotemporal dementia?

The cause of FTD is unknown. Those with a family history of the disease are more likely to develop FTD. There are patterns in individuals with FTD, such as loss of neurons and abnormal amounts or forms of proteins called tau and TDP-43. Roughly one-third of FTD cases are inherited. In these individuals, FTD is usually caused by a genetic change that affects (directly or indirectly) one of the above proteins. Genetic testing can reveal an underlying mutation responsible for FTD in about 40% of patients. The diagnosis may be confirmed after death with a brain autopsy.

What are the symptoms of frontotemporal dementia?

FTD usually begins with gradual changes in personality, behavior, or speech. People with FTD may also have motor difficulties similar to those with Parkinson’s disease (rigidity and slowness of movement), or amyotrophic lateral sclerosis (weakness). Memory loss can occur with FTD but is less obvious than in other types of dementia.

Other symptoms can include:

  • Decreased speech
  • Inability to name common objects
  • Loss of motivation
  • Lack of concern or sympathy for others
  • Inappropriate social or sexual behavior
  • Rigid, inflexible thinking
  • Compulsive, repetitive behaviors

How is frontotemporal dementia diagnosed?

Because FTD can cause changes in personality and behavior, it may be misdiagnosed as a psychiatric disorder. FTD can also be confused for Alzheimer’s disease and Parkinson’s disease. An accurate diagnosis is important and should be made after a thorough evaluation that includes:

  • A discussion of symptoms
  • Review of personal and family medical history
  • Tests of thinking, speaking, and behavior
  • A physical exam

Blood tests and brain scans are often performed, as well as genetic tests and sometimes spinal fluid testing. MRI or CT scans may show abnormalities in the frontal or temporal lobes of the brain. PET or SPECT scans may be helpful in distinguishing FTD from other causes of dementia.

What are the prognosis and treatment options?

FTD worsens over time and impairs the individual’s ability to live and function independently. Although there is no cure for FTD, there are medications that can help with some of the behavioral symptoms and improve quality of life. Speech therapy can be helpful for language difficulties. A tailored program that includes physical and occupational therapy as well as medications can improve symptoms associated with motor presentations of FTD. With an accurate diagnosis, unnecessary medications can be removed that might worsen the disease symptoms.

Where can I learn more?

More information about frontotemporal dementia can be found at:

What is Lewy body dementia?

Lewy body dementia (LBD) is a brain disease that impairs thinking and often mobility. It is the third most common cause of dementia after Alzheimer’s disease (AD) and vascular dementia. LBD accounts for up to 20% of all dementia cases in the United States.

What are the causes of Lewy body dementia?

What causes LBD is unknown, but it is not usually hereditary. In LBD, cells in the brain contain abnormal protein deposits known as Lewy bodies that contain a specific protein, alpha synuclein. These affect brain signals and disrupt brain functions. Experts are still exploring factors that are associated with, or alter the risk of, LBD:

  • Loss of smell and dream enactment behavior are associated with LBD
  • Genetics variants in several genes increase the risk of LBD
  • Lifestyle: regular exercise and healthy eating may reduce risk

What are the symptoms of Lewy body dementia?

A person with LBD may experience:

  • Thinking difficulties, including trouble with reasoning and attention
  • Visual hallucinations (“seeing” people or things that are not there)
  • Significant day-to-day fluctuations in cognitive abilities and alertness
  • Stiffness and slowness of movement (parkinsonism)
  • Tremors or shaking, most commonly at rest
  • Talking or moving during dreams
  • Mood changes, including depression, agitation and anxiety

People with LBD can also experience changes to the part of the nervous system that regulates automatic functions. These may lead to lightheadedness or fainting, and constipation, among other symptoms.

How is Lewy body dementia diagnosed?

LBD is often confused with AD or Parkinson’s disease (PD). Accurate diagnosis is critical because people with LBD have distinct symptoms that require different treatment strategies and may be sensitive to certain medications. A diagnosis of LBD is made after a thorough evaluation, which includes:

  • A discussion of symptoms
  • A physical exam
  • Diagnostic testing

Blood tests, brain scans and occasionally cerebrospinal fluid analysis are also performed. No single brain scan or medical test can definitively diagnose LBD. Recently, both a skin test and a cerebrospinal fluid test have been developed to detect the Lewy body protein, alpha synuclein, but these tests are not yet widely adopted in clinical practice. The diagnosis can be confirmed after death with a brain autopsy showing Lewy bodies.

What are the prognosis and treatment options?

LBD worsens over time and impairs the individual’s ability to live and function independently. Though there is no known cure for LBD, three types of medications may be used to treat LBD symptoms:

Cognitive

  • Cholinesterase inhibitors such as donepezil (Aricept®), galantamine (Razadyne), or rivastigmine (Exelon®) Movement
  • Medications used to treat people with PD such as carbidopa/levodopa (Sinemet®)

Sleep Disorders

  • Melatonin 

Behavioral and Mood Changes

  • Medications for visual hallucinations and behavioral problems, such as atypical antipsychotics and antidepressants

Where can I learn more?

More information about Lewy Body dementia can be found at:

What is LATE type dementia? 

LATE type dementia is a recently characterized type of dementia similar to other types of dementia in that it impairs memory and thinking. However, the causes and the overall rate of progression in LATE make it distinct from other conditions.

LATE is an acronym that stands for:

  • Limbic-predominant
  • Age-related
  • TDP-43
  • Encephalopathy

LATE occurs across a set of brain structures known as the limbic regions, considered to be one of the oldest parts of the nervous system. The limbic brain regulates emotions, behaviors, motivations, and certain aspects of memory. 

LATE typically affects people over the age of 80, and involves the abnormal buildup of a protein called TDP-43 within the limbic regions, rather than the typical amyloid plaques and tau tangles that are found in Alzheimer’s disease.

What are the causes of LATE? 

TDP-43 is an essential protein required for brain cells (neurons) to function. In LATE, the buildup of TDP-43 interferes with its normal activity, directly affecting the function of neurons in the limbic regions of the brain. This, in turn, results in the gradual loss of memory—in particular the ability to form new memories—characteristic of LATE. 

Because LATE was only recently recognized, we do not yet truly understand just how common this condition is. Nevertheless, in large studies of people over the age of 80, ~40% were found to have TDP-43 deposits, and 25% of those had experienced problems with their memory. As described below, because LATE can only be diagnosed on autopsy, it may be that LATE is much more common than we know.

What are the symptoms of LATE?

Like Alzheimer’s disease, LATE manifests itself in problems with memory, difficulty thinking and making decisions, trouble finding the right words, and wandering or getting lost.

Other symptoms can include:

  • Problems forming new memories
  • Difficulty thinking and making decisions
  • Trouble finding the right words
  • Wandering or getting lost

How is LATE diagnosed? 

Currently, there is no way to diagnose LATE in living people. It can only be diagnosed after death through autopsy. Although not truly diagnostic, neuropsychological testing can be helpful in identifying patterns of cognitive decline that are associated with LATE. In addition, MRI and PET scans can be used to eliminate other causes of dementia. If you are concerned about your memory or are experiencing other symptoms of dementia, please speak with your doctor.

What are the next steps for diagnosis and treatment?

Research focused on the investigation of causes, risk factors, and diagnostic procedures for LATE and other types of dementia continues to rely on volunteers who participate in clinical studies as well as those who donate their brains after death. 

If you might want to learn more about brain donation and our brain donation program, please contact Matthew Perkins, the Michigan Brain Bank Coordinator, at [email protected] or 734-647-7648.

Current research is focused on determining blood or imaging tests that are capable of
distinguishing LATE from other causes of dementia. Other investigators are looking into what makes the limbic regions so vulnerable to TDP-43 deposits, and why other regions of the brain are more resistant. All of these studies have the potential to not just help us recognize LATE sooner and with more confidence, but also to halt the condition with new medications and
therapeutic strategies.

Where can I learn more?
More information about LATE type dementia can be found at:

What is mild cognitive impairment?

Mild cognitive impairment (MCI) is a decline in thinking abilities that is greater than expected based on a person’s age. However, the decline does not impair the person’s ability to complete daily activities (as compared to dementia, in which the decline interferes with daily activities). It is important to recognize MCI because it puts a person at a greater risk of developing dementia in the future.

What are the causes of mild cognitive impairment?

MCI has many potential causes, not all of which are completely understood. Experts believe that many cases – but not all – result from brain changes occurring in the early stages of Alzheimer’s disease or a similar disease.

What are the symptoms of mild cognitive impairment?

Experts classify MCI based on the thinking skills affected:

Amnestic MCI

Amnestic MCI affects memory. A person with Amnestic MCI may forget information that they would have previously recalled easily, such as:

  • Appointments
  • Conversations
  • Recent events

Nonamnestic MCI

Nonamnestic MCI affects thinking abilities other than memory. A person with nonamnestic MCI may have difficulty:

  • Judging the time or sequence of steps needed to complete a complex task
  • Making sense of visual information
  • Finding or using words correctly

How is mild cognitive impairment diagnosed?

MCI is diagnosed after a thorough evaluation that includes:

  • A discussion of symptoms and ability to perform daily activities
  • Testing of memory and other thinking abilities
  • A physical exam

In addition, blood tests and brain imaging can be done to look for specific causes of MCI. In some cases, genetic or cerebrospinal fluid tests may be performed. There are now specialized blood tests and brain scans that can help determine if an individual has MCI due to Alzheimer’s disease.

What are the prognosis and options for treatment?

Over time, MCI can progress to dementia, but progression does not always occur. Depending on the cause, there may be treatments to reduce symptoms or prevent or slow progression.
Medications used to manage Alzheimer’s disease may help some individuals with MCI. 

Some studies suggest that the following may help slow decline:

  • A healthy diet
  • Exercise
  • Participation in mentally simulating and socially engaging activities

Where can I learn more?

More information about mild cognitive impairment can be found at:

What is Posterior Cortical Atrophy?

Posterior cortical atrophy (PCA) is a brain condition in which the back part of the brain (the posterior cortex) slowly deteriorates. This area helps us see and understand the world by recognizing objects, reading, judging distance, and navigating. Unlike Alzheimer’s disease (AD), memory may be maintained at first, and problems with vision-related tasks are the early signs.

What are the causes of Posterior Cortical Atrophy?

PCA is a clinical syndrome. This means it describes a pattern of symptoms and brain changes rather than a single disease. In most people, PCA is caused by Alzheimer’s disease. Many studies show that the majority of people with PCA have positive amyloid and tau biomarkers, consistent with AD. A smaller group have other causes such as Lewy body dementia, corticobasal degeneration, or (rarely) prion disease.

What is the prevalence of Posterior Cortical Atrophy?

PCA is underrecognized and definitions have varied but specialists report that roughly 5% of people with AD present with a PCA-type profile. In early-onset AD (symptoms before age 65), this can be around 8–13%. PCA most often begins between ages 50 and 65, though it can occur earlier or later.

What are the symptoms of Posterior Cortical Atrophy?

Symptoms vary across people and change over time. Early features reflect problems in the visual processing networks:

  • Difficulty reading (losing place on the page, letters seem to move or blur)
  • Trouble judging distance or depth; bumping into objects; getting lost in familiar places
  • Problems recognizing objects or seeing more than one object at a time (simultanagnosia)
  • Difficulty with spatial tasks like dressing (finding sleeves) or using tools/appliances
  • Problems with calculations, spelling, or writing
  • Hallucinations can occur in some people, especially if Lewy body disease is present
  • Memory and insight are often relatively preserved early on, but decline later

How is Posterior Cortical Atrophy diagnosed?

PCA may be missed at first because eye exams are often normal. In 2017, international experts agreed on research consensus criteria for diagnosing the PCA syndrome and describing the likely underlying disease (for example, PCA due to Alzheimer’s disease). Evaluation usually includes a neurological exam, neuropsychological testing focused on visuospatial skills, and brain imaging.

Helpful tests include:

  • MRI (often shows thinning/atrophy in occipital and parietal lobes)
  • FDG-PET (often shows reduced metabolism in posterior brain regions)
  • Tau PET and amyloid PET, or CSF/plasma biomarkers (often positive for Alzheimer’s disease in PCA)

What are the prognosis and treatment options?

PCA is progressive. Over the years, visuospatial problems usually worsen and other thinking
skills can decline, but this varies across people. There is no cure specific to PCA yet. Management focuses on symptoms, safety, and quality of life. If biomarkers show Alzheimer’s disease (the most common cause), standard AD medications are often used:

  • Acetylcholinesterase inhibitors (for mild to moderate stages)
  • Memantine (typically for moderate to severe stages)

Evidence in PCA specifically is limited, so decisions are individualized. Because many people are younger at onset, early support for work, driving, and family responsibilities is important.

Non-drug supports also matter a lot:

  • Occupational therapy and environmental changes (good lighting, high contrast labels, decluttering, clear pathways)
  • Reading aids and strategies (e.g., line guides, larger fonts, text-to-speech tools)
  • Mobility strategies (reduce shadows and visual complexity; consistent lighting)
  • Education and counseling for patients and families; driving safety and planning ahead

What is primary progressive aphasia (PPA), and what are the signs and symptoms?

PPA is a type of dementia in which language abilities are the primary symptoms. Initial cognitive symptoms include difficulty with word-finding, repetition, naming, language comprehension, and articulation. Swallowing difficulties may also be present.

How is PPA caused, and what are the risk factors? 

PPA can be caused by deposits of proteins such as tau, amyloid or TDP-43 in the brain. Damage in specific areas within the frontal, temporal, and parietal regions of the brain, along with specific language symptoms, dictates the particular type of PPA an individual may have. Some cases of PPA are inherited and have been tied to mutations in the genes GRN and MAPT.

PPA may cause changes in behavior.

Individuals with PPA are often aware of their communication difficulties, which may cause frustration, depression, anxiety, apathy or social withdrawal. Later in the disease course, behavioral problems such as impulsivity and disinhibition may occur. Movement problems like clumsiness or balance problems may also be present.

Where can I learn more?

What is vascular dementia?

Vascular dementia refers to changes to memory, thinking, and behavior that occurs when blood flow to the brain is reduced, and brain cells are deprived of oxygen and nutrients. Vascular dementia is considered the second most common cause of dementia after Alzheimer’s disease, accounting for up to 30% of cases.

What are the causes of vascular dementia?

Any condition that damages the brain’s blood vessels can lead to vascular dementia. These “vascular risk factors” include:

  • Age
  • High blood pressure
  • High cholesterol
  • Diabetes or high blood sugar
  • Smoking
  • Little or no physical exercise
  • Unhealthy diet
  • Obesity
  • Obstructive sleep apnea
  • Hardening of arteries anywhere in the body

What are the symptoms of vascular dementia?

Symptoms begin gradually or can occur suddenly, and then progress over time, with possible short periods of improvement. A person with vascular dementia may experience:

  • Trouble following instructions or learning new information and routines
  • Reduced ability to organize thoughts
  • Problems with memory
  • Changes in personality, behavior, and mood, such as depression, agitation, and anger
  • Hallucinations or delusions
  • Physical stroke symptoms such as weakness, speech changes, or trouble walking

How is vascular dementia diagnosed?

Vascular dementia is diagnosed after a thorough evaluation, which includes:

  • A discussion of symptoms (including any history of strokes)
  • A physical exam, including neuropsychological tests
  • Diagnostic testing, including a brain scan to look for vascular changes

Sometimes vascular dementia is difficult to distinguish from Alzheimer’s disease. In many cases, a person may have both vascular dementia and Alzheimer’s disease. This is referred to as mixed dementia.

What are the prognosis and treatment options?

Unfortunately, there are no treatments that can reverse the damage that has been done to the brain after it has occurred. However, physical therapy can help if there is weakness or trouble walking. Medications and lifestyle changes reduce the risk of additional vascular injury to the brain. Medications used to treat Alzheimer’s disease may also be helpful for early form of vascular dementia.

Follow these steps to reduce the risk of developing vascular dementia:

  • Don’t smoke
  • Keep a healthy blood pressure, cholesterol level, and blood sugar
  • Eat a healthy diet
  • Exercise
  • Get a sufficient amount of good quality sleep
  • Maintain a healthy weight
  • Limit alcohol consumption

Where can I learn more?

More information about vascular dementia can be found at: