Vascular dementia is the second most common form of dementia and is caused by reduced blood flow and oxygen to the brain—often from small vessel disease and/ or a stroke or series of strokes (or artery disesease).
Most commonly there is a blockage of small blood vessels somewhere in the vast system of arteries that feeds the brain and enters through the base of the skull. Blockages may be caused by plaque build-up on the inside of the artery wall, or by blood clots that have broken loose and clogged a tributary further downstream. Clots can form as a result of abnormal heart rhythms, or other heart abnormalities. Also, a weak patch on an artery wall can balloon outward and form an aneurysm, which can burst and deprive the brain cells of oxygen.
- Small vessel disease is a condition in which the small blood vessels deep inside the brain become narrowed or thickened. This can be caused by aging, high blood pressure, hardening of the arteries, diabetes, autoimmune inflammatory diseases of the arteries such as lupus and temporal arterities, or brain hemorrhage.
The brain requires oxygen supplied by blood via the vascular network to function normally. Vascular dementia results from problems with blood supply to the brain. If the vessels are damaged, blood may not be able to reach the brain cells and consequently the cells may die of oxygen starvation triggering the onset of vascular dementia. Increasingly, it seems that one particular type of vascular disease, small vessel disease, may be the major form of vascular dementia.
In the case of stroke as a cause of vascular dementia, the strokes may be in fact be so small as to be unnoticeable (mini-strokes), the damage can add up over time, leading to memory loss, confusion, and other signs of dementia. While there is no known cure, you can learn to manage symptoms, prevent further strokes, and enjoy a full, rewarding life.
The most common causes of stroke (infarction) are untreated high blood pressure (hypertension), diabetes, high cholesterol, and heart disease.
Behavioral and physical symptoms of vascular dementia can come on dramatically or very gradually, although it appears that a prolonged period of mini-strokes or interrupted blood flow leads to a gradual decline in memory, whereas a major stroke can produce profound symptoms immediately. Regardless of the rate of appearance, vascular dementia typically progresses in a stepwise fashion, where lapses in memory and reasoning abilities are followed by periods of stability, only to give way to further decline.
Vascular dementia refers to a progressive decline in memory and cognitive functioning caused by a blockage or reduction in the blood flow to the brain. When the blood supply to the brain is interrupted, brain cells are deprived of vital oxygen and nutrients, causing damage to the cortex of the brain—the area associated with learning, memory, and language. Vascular dementia is the second most common type of dementia after Alzheimer’s disease, accounting for up to 40 percent of dementia cases in older adults.
Vascular dementia refers to a progressive decline in cognitive ability resulting from brain damage from impaired blood flow to your brain. It results from a blockage or reduction of blood flow to the brain. When the blood supply to the brain is interrupted, brain cells are deprived of oxygen and nutrients, causing damage to the brain cells in the cortex of the brain—the area associated with learning, memory, and language. Decreased blood flow can damage and eventually kill cells anywhere in the body. The brain has many networks of blood vessels, so is especially vulnerable.
Vascular dementia can develop after a stroke blocks an artery in the brain, but strokes don’t always cause vascular dementia. Whether a stroke affects your thinking and reasoning depends on your stroke’s severity and location. Vascular dementia also can result from other conditions that damage blood vessels and reduce circulation, depriving your brain of vital oxygen and nutrients.
Depending on the person, and the severity of the stroke or strokes, vascular dementia may come on gradually or suddenly, and can range from mild to severe. Currently, there is no known cure for vascular dementia, but there are steps you can take to help prevent strokes, compensate for cognitive losses, and slow its development.
Multi-infarct dementia (MID) is caused by a series of small strokes (sometimes called “mini-strokes” or “silent strokes”) that often go unnoticed. These mini-strokes, also referred to as transient ischemic attacks (TIAs), result in only temporary, partial blockages of blood supply and brief impairments in consciousness or sight. Over time, however, as more areas of the brain become damaged, the symptoms of vascular dementia begin to appear. MID usually affects people between the ages of 60 to 75, and is more common in men than women.
Factors that increase your risk of heart disease and stroke — including high blood pressure, high cholesterol and smoking — also raise your vascular dementia risk. Controlling these factors can help lower your chances of developing vascular dementia.
In this pattern, changes in your thought processes occur in noticeable steps downward from your previous level of function, unlike the gradual, steady decline that typically occurs in Alzheimer’s disease.
There may be long periods of stability until the next vascular event which then produces another noticeable stage of decline, followed again by a long period of stability until the next event. (LP)
But vascular dementia can also develop very gradually, just like Alzheimer’s disease. What’s more, vascular dementia and Alzheimer’s often occur together.
Symptoms can vary widely, depending on the severity of the blood vessel damage and the part of the brain affected. Memory loss may or may not be a significant symptom depending on the specific brain areas where blood flow is reduced.
Vascular dementia symptoms include:
- Trouble speaking of understanding words/speech
- Trouble paying attention and concentrating
- Reduced ability to organize thoughts or actions
- Decline in ability to analyze a situation, develop an effective plan and communicate that plan to others
- Difficulty deciding what to do next
- Problems with memory
- Restlessness and agitation
- Unsteady gait
- Sudden or frequent urge to urinate or inability to control passing urine
Multiple small strokes or other conditions that affect blood vessels and nerve fibers deep inside the brain may cause more gradual thinking changes as damage accumulates. Common early signs of widespread small vessel disease include impaired planning and judgment; uncontrolled laughing and crying; declining ability to pay attention; impaired function in social situations; and difficulty finding the right words.
High blood pressure, high cholesterol, or other risk factors for heart or blood vessel disease put one at risk of developing Vascular Dementia.
Advancing age is a major risk factor for vascular cognitive impairment or dementia.
Additional risk factors are the same ones that raise risk for heart problems, stroke and other diseases that affect blood vessels. Many of these vascular factors also raise risk for Alzheimer’s. The following strategies may reduce your risk of diseases that affect your heart and blood vessels — and also may help protect your brain:
- Don’t smoke
- Keep your blood pressure, cholesterol and blood sugar within recommended limits
- Eat a healthy, balanced diet
- Maintain a healthy weight
- Limit alcohol consumption
The U.S. Food and Drug Administration (FDA) has not approved any drugs specifically to treat symptoms of vascular dementia, but there is some clinical trial evidence that certain drugs approved to treat Alzheimer’s may also offer a modest benefit in people diagnosed with vascular dementia.
Controlling risk factors that may increase the likelihood of further damage to the brain’s blood vessels is an important treatment strategy. There’s substantial evidence that treatment of risk factors may improve outcomes and help postpone or prevent further decline.
Like other types of dementia, vascular dementia shortens lifespan. Some data suggest that those who develop dementia following a stroke survive three years, on average. As with other stroke symptoms, cognitive changes may sometimes improve during recovery and rehabilitation from the acute phase of a stroke as the brain generates new blood vessels and brain cells outside the damaged region take on new roles.
Vascular brain changes can coexist with other types of dementia. Therefore, some people may have both vascular dementia and another form of dementia.
Vascular dementia is widely considered the second most common cause of dementia after Alzheimer’s disease, accounting for 20 to 30 percent of cases. Many experts believe that vascular dementia remains underdiagnosed even though it is very common. Vascular dementia is also commonly mistaken for Alzheimers, especially when the part of the brain affected is the part associated with memory.
A growing number of experts prefer the term “vascular cognitive impairment (VCI)” to “vascular dementia” because they feel it better expresses the concept that vascular thinking changes can range from mild to severe.
Vascular Dementia Causes:
Vascular dementia results from conditions that damage your brain’s blood vessels, reducing their ability to supply your brain with the amounts of nutrition and oxygen it needs to perform thought processes effectively.
Common conditions that may lead to vascular dementia include:
- Stroke (infarction) blocking a brain artery. Strokes that block a brain artery usually cause a range of symptoms that may include vascular dementia. But some strokes don’t cause any noticeable symptoms. These “silent brain infarctions” still increase dementia risk.With both silent and apparent strokes, the risk of vascular dementia increases with the number of infarctions that occur over time. One type of vascular dementia involving many strokes is called multi-infarct dementia.
- Narrowed or chronically damaged brain blood vessels. Conditions that narrow or inflict long-term damage on your brain blood vessels also can lead to vascular dementia. These conditions include the wear and tear associated with aging; high blood pressure; hardening of the arteries; diabetes; lupus erythematosus; brain hemorrhage; and temporal arterities.
Risk Factors for Vascular Dementia
- Increasing age. Vascular dementia is most common in those over the age of 65. Risk increases the older you get. The disorder is rare before age 65, and risk rises substantially as you reach your 80s and 90s.
- History of heart attack, strokes or mini strokes. If you’ve had a heart attack, you may be at increased risk of having blood vessel problems in your brain. The brain damage that occurs with a stroke or a mini stroke (transient ischemic attack) may increase your risk of developing dementia.
- Atherosclerosis occurs when deposits of cholesterol or plaques build up in the arteries and narrow blood vessels, reducing blood flow to the brain. Atherosclerosis increases the risk of vascular dementia — and possibly of Alzheimer’s disease — by reducing the flow of blood that nourishes your brain.
- High cholesterol. Elevated levels of low-density lipoprotein (LDL), the so-called “bad” cholesterol, are associated with an increased risk of vascular dementia, and possibly with a higher risk of Alzheimer’s disease.
- High blood pressure. Doctors estimate that about 50 percent of cases of vascular dementia result from hypertension. High blood pressure places extra stress on blood flow throughout the body, including the brain. When your blood pressure’s too high, it puts extra stress on blood vessels everywhere in your body, including your brain. This increases the risk of vascular problems in the brain.
- Diabetes. High glucose levels damage blood vessels throughout your body. Damage in brain blood vessels can increase your risk of stroke and vascular dementia.
- Smoking. Smoking directly damages your blood vessels, increasing your risk of atherosclerosis and other circulatory diseases, including vascular dementia.
- Obesity. Being overweight is a well-known risk factor for vascular diseases in general, and therefore, presumably increases your risk of vascular dementia.
- Atrial fibrillation. In this abnormal heart rhythm, the upper chambers of your heart begin to beat rapidly and irregularly, out of coordination with your heart’s lower chambers. Atrial fibrillation (abnormal heart rhythm) can reduce blood flow to the brain and increase the risk of blood clots forming.
|Common Signs and Symptoms of Vascular Dementia|
|Mental and Emotional Signs and Symptoms|
|Physical Signs and Symptoms|
|Behavioral Signs and Symptoms|
Know the symptoms of stroke
Call 911 immediately if you experience any of the following symptoms, which may indicate you’ve had a stroke or a transient ischemic attack (TIA), or mini-stroke.
- Numbness, paralysis, or weakness on one side of your body or face
- Trouble speaking (e.g. slurring your words, inability to repeat a simple sentence)
- Loss of vision or seeing double
- Loss of balance and coordination (e.g. dizziness, trouble walking)
- Sudden, severe headache (may include a stiff neck, vomiting, or pain between your eyes)
It’s important to act quickly. Prompt treatment may be able reopen a blocked blood vessel and reduce the severity of the stroke.
Lower your risk for vascular dementia by reducing your risk for stroke
- Know your blood pressure. If high, work with your doctor to lower it.
- Find out from your doctor if you have atrial fibrillation.
- If you smoke, stop.
- If you drink alcohol, do so in moderation.
- Find out if you have high cholesterol. If so, work with your doctor to control it.
- If you are diabetic, follow your doctor’s recommendations carefully to control your diabetes.
- Include exercise in the activities you enjoy in your daily routine.
- Enjoy a lower sodium (salt), lower fat diet.
Source: National Stroke Association
Vascular dementia diagnosis and treatment
Symptoms of vascular cognitive impairment can often go unrecognized, so if you’ve suffered a stroke, mini-stroke, or have other risk factors for heart or blood vessel disease, your doctor may recommend cognitive tests. If initial screening tests suggest cognitive changes, your doctor may embark on a more detailed assessment of thinking skills such as judgment, planning, problem-solving, reasoning, and memory. This assessment may also include brain scans and tests to rule out other causes of your symptoms.
To make a diagnosis, your doctor may also seek input from family members or trusted friends about any subtle changes they’ve noticed in your behavior or cognitive abilities.
Treating vascular dementia
While there is currently no cure for vascular dementia, the earlier any brain damage is caught, the better your chance of preventing dementia, or at least slowing down the progression of the disease. By treating the risk factors that led to vascular dementia, such as high blood pressure or diabetes, you may even be able to reverse some of the symptoms.
Physiotherapy, occupational therapy, speech therapy can help you to regain some or all of any lost functions following a stroke. A number of medications used to treat the cognitive symptoms of Alzheimer’s disease appear to work for vascular dementia, too, but the most important thing is to minimize your risk of having another stroke and making the dementia worse. Your doctor may prescribe medications to lower blood pressure and prevent clots from forming, and may change or stop medications that can exacerbate symptoms of dementia, such sedatives, antihistamines, or strong painkillers. However, adopting healthier lifestyle changes is also a vital part of vascular dementia treatment. This means eating right, losing weight, exercising, getting high blood pressure under control, avoiding cigarettes, and controlling cholesterol levels and diabetes.
Helping someone with vascular dementia
Caring for a person with vascular dementia can be very stressful for both you and your loved one. You can make the situation easier by providing a stable and supportive environment. Modify the caregiving environment to reduce potential stressors that can create agitation and disorientation in a dementia patient. Avoid loud or unidentifiable noises, shadowy lighting, mirrors or other reflecting surfaces, garish or highly contrasting colors, and patterned wallpaper. Use calming music or play the person’s favorite type of music as a way to relax the patient when agitated.
A stable environment starts with a stable, healthy you. It’s easy to lose sight of your own needs when your loved one is dealing with dementia. But taking care of yourself isn’t optional. Stress and burnout are common in caregivers—and that isn’t a good thing for you or the person you’re caring for. Nurturing and protecting your own emotional and physical health isn’t selfish. It’s the best thing you can do for the person you love. Getting anxious or upset can increase your loved one’s stress or agitation. Try to remain flexible, patient, and relaxed. If you find yourself becoming anxious or losing control, take a time out to cool down. Try not to take problem behaviors personally and do your best to maintain your sense of humor.
Tips for caring for a loved one with vascular dementia
- Create a routine. Your loved one will feel more comfortable and less agitated when he or she is on a regular routine and in familiar surroundings.
- Use calendars and clocks. Place large calendars and clocks around your loved one’s living area. They can help people with dementia reorient if they’ve forgotten the date or time.
- Keep your loved one busy. Encourage your loved one to continue physical and social activities as long as possible. Whether it’s going for a walk or spending time at the local senior center, it’s important that he or she has regular activities to participate in. Simple daily chores like folding laundry, watering plants, or peeling vegetables can help keep your loved one busy.
- Provide plenty of stimulation. Make sure your loved one’s room is colorful and inviting. Is there a nice view outside? If not, you can bring the outdoors inside with some flowers or a plant. Exercise, interaction with different people in one-on-one situations, or playing with a well-trained, docile pet can also help to provide stimulation and increase physical and social activity.
- Be sure to communicate, even if you’re not sure your loved one understands. If it’s time for dinner, for example, say so. Don’t just lead your loved one into the kitchen without explaining what’s going on. Even if he or she doesn’t understand your words, use your tone of voice, eye contact, a smile, or a reassuring touch to help convey your message and show your compassion.
From the University of Toronto:
Vascular dementia (VaD) is the second most prevalent subset of dementia next to Alzheimer’s Disease (AD). VaD can result from any condition that damages the vascular system of the brain. The vascular system supplies the brain with blood filled with oxygen and nutrients which are vital to the brain’s function. Damage to the vascular system system results in hypoperfusion (reduced blood flow to the brain). Hypoperfusion may eventually lead to the loss of brain cells, and the onset of VaD.
The brain damage which causes VaD cannot be reversed. As a result, most treatments aim to slow or prevent the progression of the disease. Prevention of VaD can be accomplished by treating pre-existing conditions which are able to cause vascular damage. These conditions include hypertension, diabetes, stroke, and heart problems. In particular, hypertension is a major risk factor for VaD independent of its role as a risk factor for stroke. Hypertension can be controlled by way of lifestyle changes and medications; therefore, implementation of these interventions in hypertensive individuals can decrease their risk for VaD. Damage to the vascular system induced by hypertension includes inflammation and oxidative stress in blood vessels. One of the major contributors to oxidative stress in the brain is thought to be nicotinamide adenine dinucleotide phosphate (NADPH) oxidases. NADPH oxidases are a class of enzymes which generate reactive oxygen species (ROS). Since this discovery, NADPH oxidase inhibitors have been examined as potential treatments for the reduction of damage caused by oxidative stress.
They are most often the result of degenerative vessel disorders which cause lesions in the brain. These vessel disorders include atherosclerosis of the cerebral arteries, cerebral small vessel disease, and cerebral amyloid angiopathy (CAA). Atherosclerosis is the accumulation of cholesterol, proteins and lipids in large and medium sized artery walls which calcify into plaques. Plaque buildup results in stenosis of the artery causing hypoperfusion to the brain. Plaques are also at risk of rupturing and inducing thrombosis (blood clot formation). The types of infarcts caused by atherosclerosis are diverse. Small vessel disease results from atherosclerosis, arteriolosclerosis and lipohyalinosis of the small vessels. Small vessel disease can cause lacunar and micro-infarcts which damage the basal ganglia, peripheral white matter, and thalamic and cerebellar white matter vessels. CAA is caused by deposits of beta amyloid protein in the wall of cerebral blood vessels. It can lead to the rupture of vessel walls, hemorrhage, micro-bleeds, capillary occlusion and blood flow disturbances in the brain.
The sporadic forms of VaD are characterized by the type of lesions they create in the brain. The characterizations include multi-infarct dementia, strategic infarct dementia, and subcortical vascular encephalopathy (Binswanger’s Disease). Multi-infarct dementia is the result of multiple micro-infarcts, large infarcts or lacunar infarcts in the gray matter of the brain. Strategic infarcts occur when there is an infarct in a specific region of the brain needed for cognitive function. The behavioural impairment resulting from the infarct is specific to the brain region damaged. For example, an infarct in the hippocampus would result in memory loss. Subcortical vascular encephalopathy results from lesions in the white matter of central and peripheral areas of the brain.
Hypertension as a Risk Factor
Hypertension is defined as an elevation in blood pressure above 140 mmHg systolic and 90 mmHg diastolic pressure. It is a major risk factor for both VaD and AD in the elderly due to the changes it makes to both the structure and function of cerebral blood vessels. Structural changes made to the vessels act in concert to reduce the lumenal diameter of cerebral blood vessels, and harden blood vessel walls. This, in turn, attenuates the ability of the cerebral blood vessels to carry out normal functions including functional hemodynamic responses, autoregulation, and endothelium-dependent responses.
Changes to Cerebral Blood Vessel Structure
|Hypertension’s Effects on Vascular Structure|
|Different structural changes made to the vascular structure and the types of infarcts they cause.|
The normal structure of cerebral blood vessels are degenerated by vessel disorders induced by hypertension such as atherosclerosis and lipohyalinosis. Lipohyalinosis is the fibrinoid necrosis of vascular walls resulting in vessel wall thickening and lumen narrowing. It most often affects vessels which supply the white matter of the brain, and can result in white matter strokes or brain hemorrhages. Both atherosclerosis and lipohyalinosis can cause occlusions in the cerebral vasculature, which can lead to ischemic injury.
Furthermore, hypertension causes hypertrophic and eutrophic remodelling of the cerebral arteries. Hypertrophic remodelling describes a process in which the thickness of the cerebral artery wall is increased; consequently, the diameter of the lumen is reduced. This is a direct result of the vascular smooth muscle cells undergoing hypertrophy. Eutrophic remodelling describes the narrowing of the vessel lumen due to the movement of smooth muscle cells, without a change in the thickness of the vessel wall. Alterations to the composition and structure of the vascular walls by these mechanisms have profound negative effects on the function of the vessels.
Changes to Cerebral Blood Vessel Function
|Hypertension’s Effects on Vascular Function|
Changes made to the structure of cerebral blood vessels reduce cerebral blood flow (CBF) and impair their adaptive responses. Adaptive responses of cerebral blood vessels ensure that the energy needs of the brain are met by way of proper CBF. Proper CBF is essential due to the brain’s dependence on a constant supply of oxygen and energy from the blood. The adaptive responses attenuated in the event of chronic hypertension include functional hyperemia, autoregulation, and endothelium-dependent vasodilation. Functional hyperemia is the increase in blood flow to active regions of the brain. This function is controlled by the neurovascular unit made up of neurons, glia and vascular cells . Hypertension disrupts the neurovascular unit which results in hypoperfusion during cognitive activation. This effect contributes to neuronal dysfunction, and leads to cognitive deficits. Endothelium dependent vasodilation refers to the ability of endothelial cells to respond to physiological stimuli through the production of vasodilators or vasoconstrictors in order to regulate arterial vascular tone. Nitric oxide (NO) is a vasodilator which is a key regulator of vascular tone. In hypertensive individuals NO availability decreases which can cause endothelial dysfunction. Cerebrovascular autoregulation is one’s ability to maintain CBF in response to changing arterial pressures. In a hypertensive individual, a higher blood pressure is required to maintain a normal range of CBF. Poor autoregulation can increase the susceptibility of white matter to damage during changes in blood pressure. It could also result in a more extreme brain injury after ischemia because the vessels need proper autoregulation to respond to the reduction in blood flow.
Damage to the Brain by Oxidative Stress
In the brain, proper function of cells is reliant on the balance between ROS generation and degeneration. When this balance is disrupted by an increase in ROS generation, a state of oxidative stress ensues. The brain has multiple sources of ROS; however, it has been shown that membrane bound NADPH oxidase enzymes are the primary sources of ROS during hypoperfusion, stroke and hypertension. In both humans and animal models of hypertension, these enzymes are shown to be overactive. Overactivity of NADPH oxidases increases the number of ROS which results in a state of oxidative stress. In a hypertensive state, the NOX2 homolog of NADPH oxidase has been implicated as the source of the increased number of ROS.
Oxidative stress has been shown to play a large role in the cerebrovascular dysfunction underlying VaD. Oxidative stress in brain vasculature impairs endothelium dependent responses which may increase one’s susceptibility to cell dysfunction, cell death, and dementia. NOX2 generates a type of ROS called superoxide anions which bind to and inactivate NO. NO is a vasodilator made by endothelium nitric oxide synthase (eNOS) in endothelial cells. The inactivation of NO reduces the amount of NO available to the cells. Reduced NO availability alters the resting tone of vessels, and endothelium-dependent vasodilation. It can also lead to hypertrophy in cerebral arterioles and arteries. Furthermore, an oxidant called peroxynitrite is formed when NO reacts with superoxide anions.Peroxynitrite inactivates antioxidant enzymes which sustains an increased level of ROS. Peroxynitrite also plays a role in eNOS uncoupling, which is a process that has been implicated in endothelial dysfunction caused by oxidative stress. eNOS requires the cofactor tetrahydrobiopterin (BH4) to synthesize NO from its precursor, L-arginine. In a state of oxidative stress, BH4 is oxidized by peroxynitrite and eNOS begins reducing oxygen to make superoxide anions instead of reducing L-arginine to make NO. This perpetuates the effects of oxidative stress in the brain by further increasing the number of oxidants.
There are currently no approved drug treatments for VaD. Some clinical trials have shown that drugs that are effective for AD, such as acetylcholinesterase inhibitors, may also be useful in the treatment of VaD. Treatments for VaD primarily aim to prevent the recurrence of vascular injury or minimize further damage to the brain. This is done through the use of antihypertensive and anti-platelet medications.
Potential Treatment: NADPH Oxidase Inhibitors
A lot of research has focused on the contribution of NADPH oxidases to oxidative stress in models of hypertension, aging, and stroke. It has been determined that overactivity of NADPH oxidases play a major role in oxidative stress induced damage to the brain. This was demonstrated in a study by Chen et al. in which mice with a NOX2 subunit knockout, and mice treated with a NOX2 inhibitor (apocynin) had less oxidative stress and inflammation after ischemia in comparison to wildtype mice. Furthermore, the infarction volume of the mouse brains reflected the reduction in oxidative stress. In knockout and apocynin treated mice, the infarction volume was much lower than in wildtype mice. These results show that NOX2 has a substantial role in mediating oxidative damage to the brain. They also show the potential of NADPH oxidase inhibitors such as apocynin to be used clinically as treatment to reduce oxidative damage following stroke. In order to determine if NADPH oxidase inhibitors could be used as treatment for VaD, a relationship between cognitive function and NADPH oxidase inhibition needs to be found.
As it stands, NADPH oxidase inhibitors appear to have the potential to prevent and reduce damage induced by oxidative stress. Oxidative stress underlies the endothelial dysfunction induced by hypertension. Consequently, NADPH oxidase inhibitors could be used to prevent VaD by reducing the negative effects hypertension has on the brain. Because NADPH oxidase inhibitors target the effects of hypertension which precede the initial onset of the VaD, they may be able to prevent initial damage to the brain. This is especially important in the case of VaD because the vascular damage which causes VaD cannot be reversed. Furthermore, there is a great need for a VaD treatment because a treatment which helps to prevent VaD could reduce morbidity and healthcare costs while improving quality of life in the growing elderly population.
http://neurowiki2014.wikidot.com/individual:pathology-of-vascular-dementia (U of Toronto)