Everything You Need to Know About Vascular Dementia

Vascular Dementia

Vascular dementia is the second most common cause of dementia in older adults after Alzheimer’s disease, accounting for approximately 15-20% of dementia cases. This disorder, also known as multi-infarct dementia, refers to the cognitive changes due to conditions that affect the blood vessels in the brain and impair the blood flow to different portions of the brain. Consequently, the lack of oxygen and nutrients due to inadequate blood supply damages and kills the brain cells, which results in significant damage and loss of these cells. The loss of brain function and cognition typically depends on the location, size, and number of vascular changes.

What causes Vascular Dementia?


A sudden stroke can sometimes trigger changes in thinking, leading to vascular dementia due to the blockage of a major blood vessel in the brain. These changes can be mild at first and may progressively worsen and cause widespread damage due to multiple minor strokes or any other condition that affects smaller blood vessels. Many experts use the term “vascular cognitive impairment” (VCI) rather than “vascular dementia” to better express the notion of mild to severe changes in vascular thinking. It is essential to know that stroke can increase the risk of developing dementia. It does not necessarily cause vascular dementia.

Changes in White Matter

Some other common brain abnormalities in people with vascular dementia include diseased small blood vessels and changes in white matter. This white matter (or connecting wires) is responsible for the conduction of neural messages between parts of the brain.

The Brain-Heart Connection

Researchers are investigating the role of these changes and their underlying causes in the onset and development of vascular dementia. Their research suggests a strong relationship between cardiovascular disease and cerebrovascular disease and the ensuing cognitive impairment and dementia. This field of research is known as “vascular contribution to cognitive impairment and dementia” (VCID). It is helping scientists better comprehend this connection and whether the prevention and treatment of cerebrovascular and heart disease could also aid in impeding dementia. VICD research includes investigating various blood flow interrupting conditions, such as hemorrhages (bleeding from damaged blood vessels), infarcts (portions of dead tissue due to inadequate blood supply), cerebral hypoperfusion (impaired blood flow), and small vessel disease (associated with white matter abnormalities and stroke).

What are the signs and symptoms of vascular dementia?

The symptoms of vascular dementia initiate gradually or occur suddenly and worsen as the disease progresses over time, with possible brief spans of improvement. Vascular dementia can also co-exist with other dementia, such as Lewy body dementia and Alzheimer’s disease. During diagnosis, its symptoms may be similar to Alzheimer’s because the vascular deterioration begins in the brain areas responsible for storing and recovering information, leading to memory loss (similar to Alzheimer’s disease).

The patient may show the most apparent symptoms shortly after a major stroke. Vascular dementia patients may exhibit the following signs:

  • Difficulty carrying out previously easy tasks
  • Getting lost on familiar routes
  • Trouble learning new information or following directions
  • Difficulty with language, reading, and writing
  • Forgetting past or recent events
  • Sleep disturbances
  • Misplacing items
  • Loss of interest in people or things
  • Hallucinations and delusions
  • Personality and behavioral changes
  • Poor judgment and loss of ability to perceive danger

How is vascular dementia diagnosed?

In 2011, the American Heart Association and American Stroke Association issued a joint scientific statement on vascular contributions to mild cognitive impairment (MCI) and dementia. According to the diagnostic approach recommended in the statement, the following criteria can suggest the highest probability that vascular changes are the cause of MCI or dementia:

1. Neurocognitive testing confirms the diagnosis of MCI or dementia. These computerized tests provide a comprehensive assessment of particular cognitive skills (memory, reasoning, judgment, and problem-solving).

2. An MRI (magnetic resonance imaging) scan of the brain to confirm a recent stroke or other vascular brain changes. The pattern and severity of the affected tissues should be coherent with the kinds of impairment reported in cognitive testing.

3. There is no evidence of the involvement of nonvascular factors in cognitive decline.

The statement also mentions that discrepancies in these criteria may imply a probability rather than a strong possibility that vascular factors are responsible for these cognitive changes.
Vascular dementia often remains undetected. Therefore, many experts recommend professional cognitive screening for individuals at a higher risk of disease development. These individuals include those who have had a stroke or a ministroke (transient ischemic attack – TIA) or those with an increased risk of developing vascular diseases.

Treatment of Vascular Dementia

Although the FDA has not particularly approved any drug for the treatment of vascular dementia, clinical trials suggest the usage of approved Alzheimer’s drugs may be an effective treatment against it. The treatment principally involves addressing the underlying disease such as hypertension, diabetes mellitus, and hyperlipidemia to prevent the progression and worsening of vascular dementia.

Another strategy is to control the risk factors associated with the possible increased risk of disease development. Research significantly suggests that treating risk factors can help prevent further cognitive decline.

People with vascular dementia should talk to their health care providers to devise the best treatment plan according to their circumstances and symptoms.

What is the lifespan of people with vascular dementia?

Vascular dementia shortens the lifespan of the affected individuals, just like other types of dementia. Research suggests that individuals who develop vascular dementia it after a stroke may live up to an average of three years.

Aducanumab Therapy for the Treatment of Alzheimer’s Disease

Treatment Of Alzheimer’s Disease

Finding an effective treatment of Alzheimer’s, a devastating disease affecting about 6.2 million people in the US, is one of the primary goals of the research world. Scientists are trying to uncover the underlying biological processes of this disease in order to discover ways to slow its progression or alleviate its symptoms. In such an attempt, the US Food and Drug Administration approved a new drug, Aduhelm (aducanumab), via an accelerated approval pathway on June 7, 2021. It is the first new treatment approved since 2003.

How does aducanumab work?

Aduhelm is the first ever disease-modifying drug or therapy to address the fundamental disease process. It is a human antibody (or immunotherapy) that targets and removes the hallmark of Alzheimer’s disease, the beta-amyloid protein. Accumulation of this protein into plaques may result in cell death and tissue loss in parts of the brain responsible for memory, reaoning, learning, and behavior. Therefore, this therapy may effectively reduce cognitive and functional impairment in people with early-stage Alzheimer’s by removing plaques from the brain.

At what stages of the disease is it prescribed?

In the clinical studies, the researchers studied the effectiveness of this new drug only in people with early-stage Alzheimer’s or mild cognitive impairment (MCI). Therefore, doctors will only prescribe it in these stages of the disease. No data is available to demonstrate its effectiveness or safety in earlier or later stages. Research is still underway to determine if this drug affects a person’s rate of cognitive decline over time.

How is aducanumab administered?

Aducanumab is an intravenous drug delivered via a 45-to-60-minute infusion every four weeks. Intravenous (IV) administration helps the drug reach the brain most effectively.

Is any diagnostic test required before its prescription?

According to the FDA, no diagnostic test is necessary before prescribing aducanumab. However, due to the fact that it targets the beta-amyloid protein in the brain, doctors may require a PET scan or a CSF (cerebrospinal fluid) analysis in order to determine the presence of plaques in the brain. These diagnostic tests assist them in making a precise diagnosis before prescribing the drug. While the patient is on aducanumab, doctors may routinely recommend MRI to oversee the possible side effects, including bleeding or swelling in the brain.

What are the side effects?

During the aducanumab treatment, there is a possibility of developing amyloid-related imaging abnormalities (ARIA) in the brain, particularly as temporary swelling in parts of the brain portions. However, the issue usually resolves itself over time, and most people do not exhibit symptoms. Some people may also experience bleeding in the brain with swelling. Other common side effects include headache, dizziness, falls, confusion, nausea, diarrhea, disorientation, and vision changes. Furthermore, there is also a potential risk of hypersensitivity reactions such as urticaria and angioedema.

Can it be taken with other medication or supplements?

It is essential to have a conversation about one’s health condition, medications, and supplements with a doctor whenever one considers any treatment, including aducanumab, in order to confirm eligibility for that treatment.

Congress announced $289 million increase in funding for Alzheimer’s research

Funding For Alzheimer’s Research

Alzheimer’s disease is the fifth leading cause of death in the U.S., killing approximately 80,000 people each year. According to some estimates, 1 in 3 older people die due to Alzheimer’s and other related dementia.

In 2020, caring for Alzheimer’s patients cost the nation over $305 million, which is expected to increase to $20 trillion (including $15 trillion to Medicaid and Medicare) in the next 40 years. For every $28,000 the federal government spends caring for Alzheimer’s patients, it allocates only $100 for Alzheimer’s disease research.

Considering that Alzheimer’s is the only disease among the top ten causes of death in America with no known cure, Alzheimer’s disease research has become a priority. Being able to conduct quality research is essential in order to identify both its underlying processes to find an effective treatment as well as ways to slow its progress. These undertakings require adequate funding. However, the federal funding of $498 million is inadequate and does not reflect the urgency of the ever increasing number of Alzheimer’s cases in the U.S.

On March 9, 2022, Congress leaders announced an increase of $289 million in the funding for Alzheimer’s and dementia-related research at the National Institute of Health (NIH) for the fiscal year 2022. The primary purposes of this increase are to provide improved care to the patients, create better treatment options, and research ways to prevent the disease.

What Does the Alzheimer’s Research Association Do?

Alzheimer’s Research Association aims to support the caregivers of Alzheimer’s disease by providing the latest news and information regarding Alzheimer’s disease and utilizing its research, donations, and grants to help people stay informed and to help them cope with their emotional and financial difficulties. We work to make the caregiving experience as rewarding as possible for the caregivers.

Caregiving for Alzheimer’s disease and dementia can be overwhelming. If you are a caregiver and are struggling with financial or emotional instabilities associated with being a caregiver, then you can contact us (through the link below). We have helpful information and tips regarding caregiving and also provide grants to try to ease your financial burden.

Contact us if you have further questions or if you would like to apply for grants!

Lewy Body Dementia: Symptoms & Diagnosis

Lewy Body Dementia: Symptoms & Diagnosis

Lewy body dementia (LBD) affects over a million individuals in the United States. Many experts consider it the third most common cause of dementia after Alzheimer’s disease and vascular dementia, consisting of 5-10% of the total cases. Its symptoms typically appear at the age of 50 or above, and it is slightly more prevalent in men than in women.

LBD was first described in 1912 when a German doctor, Dr. Frederich H. Lewy, discovered neuronal inclusions in the brain of people with Parkinson’s disease while working in Dr. Alois Alzheimer’s laboratory. These inclusions or protein clumps, which were then named “Lewy bodies” after him, are a tell-tale sign of Lewy body dementia.

The formation and deposition of Lewy bodies occurs in the neurons of the brain portions responsible for memory, thinking, behavior, and movement. They are chiefly composed of alpha-synuclein proteins that induce chemical changes in the brain, leading to cognitive decline. Although it is abundantly present in the brain, its general function is still unknown.

What causes Lewy body dementia?

It is still unclear what causes Lewy body dementia. Researchers are learning more about its biology and the impact of genetics in order to determine possible causes and risk factors. Studies suggest that the build-up of Lewy bodies results in the loss of neurons responsible for the production of two important neurotransmitters (chemicals that conduct messages between neurons) viz, acetylcholine and dopamine. The former is crucial for memory and learning, while the latter is involved in cognition, movement, behavior, motivation, mood, and sleep.

Researchers have identified various risk factors of Lewy body dementia, among which age is the most prominent factor. Certain health conditions and diseases, particularly Parkinson’s disease and REM sleep behavior disorder, can also increase an individual’s risk of developing LBD.

Family history may also be a risk factor, but LBD is not a genetic disorder. Scientists have reported variants in three genes, APOE, SNCA, and GBA, linked with an increased LBD risk. The cause is, however, not known in most cases.

What are the Signs and Symptoms of Lewy Body Dementia?

Since LBD is a progressive disorder, it slowly develops and worsens with time. A person usually lives up to an average of five to eight years after diagnosis. However, some people may live from two to twenty years.

Similar to Alzheimer’s disease, LBD develops in stages. Symptoms are mild during the early stages, and people usually exhibit relatively normal functioning. However, As the disease progresses, movement and cognition continue to decline. At the late stage, people may become entirely dependent on others for assistance and care.

The development and progression of LBD varies greatly from individual to individual and is contingent on certain factors such as age, health, and severity of symptoms. LBD patients may not experience all the symptoms of the disease. Should a person exhibit a sudden functional or behavioral change, it should be reported to a doctor. The primary symptoms of the disease are changes in cognition, movement, sleep, and behavior.

● Cognitive Symptoms

Lewy body dementia can cause severe cognitive impairment that interferes with daily activities. LBD may seem similar to Alzheimer’s dementia in this regard, but unlike Alzheimer’s, these memory changes may not initially be apparent. Instead, they may arise with it’s progression. The cognitive symptoms include:

  1. Visual hallucinations and sometimes, non-visual (auditory, olfactory, or tactile) hallucinations
  2. Changes in concentration, alertness, and attention that vary throughout the day or from one day to another
  3. Disorganized and unclear ideas
  4. Severe cognitive impairment that often arises with any disease progression
  5. Poor judgment and confusion
  6. Difficulty with language and numbers

● Changes in Movement

Movement problems vary from person to person. Some people may not significantly experience these symptoms for several years, while others may develop them even in the earlier stages of LBD. These symptoms include:

  1. Stiff muscles
  2. Balance problems with frequent falls
  3. Stooped posture
  4. Tremors or shaking, particularly during rest
  5. Slow movement and shuffling walk
  6. Swallowing problems
  7. Loss of coordination

● Changes in Sleep

Although sleep problems are widespread in LBD patients, they are generally undiagnosed. Following are the sleep changes that a person with LBD may experience:

  1. REM sleep behavior disorder (which involves physically acting out dreams while sleeping)
  2. Insomnia
  3. Too much sleep during daytime
  4. Restless leg syndrome (characterized by an overwhelming urge of moving legs when at rest)

● Behavioral Symptoms

People with LBD may experience behavioral and mood changes that may worsen with declining cognitive functioning. The symptoms include:

  1. Depression and anxiety
  2. Apathy and loss of motivation
  3. Agitation and restlessness
  4. Delusions, suspicion, and paranoia

Diagnosis of Lewy Body Dementia

Currently, there is no single test for precisely diagnosing Lewy body dementia. Since its symptoms resemble other types of dementia, such as Alzheimer’s disease and Parkinson’s disease, it becomes difficult to diagnose, particularly in the early stage. The doctors can make the diagnosis with their professional judgment of the symptoms.

Many scientists consider Lewy body dementia and Parkinson’s disease dementia to be two different interpretations of the same fundamental problems arising from the brain’s, processing of the alpha-synuclein protein. However, most experts suggest diagnosing them as distinct disorders.

The diagnosis is LBD when:

  • Dementia symptoms related to LBD develop first.
  • Movement changes and dementia symptoms are diagnosed simultaneously
  • The symptoms of dementia emerge within one year after movement symptoms.

On the other hand, the diagnosis is Parkinson’s disease dementia should an individual, who is already diagnosed with Parkinson’s due to manifestation of movement symptoms, does not exhibit dementia symptoms until after a year or more.

However, due to the co-existence of Lewy bodies with Alzheimer’s brain changes, distinguishing LBD from Alzheimer’s disease may sometimes become challenging, particularly in the early stages.

For diagnosis of LBD, doctors may recommend a few tests such as a neurological and physical examination, blood tests to check hormone levels, assessment of mental abilities, brain scans (an MRI or CT scan), and sleep evaluation.