Dementia is the basic term for loss of memory and other mental abilities severe enough to interfere with daily living. It is caused by physical changes in the brain. Dementias other than Alzheimer’s disease account for 30-50% of cases. Below is a list of other types of dementias:
Vascular Dementia (VD) is the second most common type of dementia, after Alzheimer's, accounting for up to 20% of all dementias. VD is generally not a progressive degenerative disease, but it rather develops when impaired blood flow to parts of the brain, from cerebrovascular or cardiovascular problems - usually strokes, deprives cells of food and oxygen, causing nerve cell and brain damage. Other underlying reasons can be genetic diseases, endocarditis (infection of a heart valve), or amyloid angiopathy (amyloid protein builds up in the brain's blood vessels, sometimes causing hemorrhagic or "bleeding" strokes). In many cases, it may coexist with Alzheimer's. Symptoms of vascular dementia often begin suddenly, frequently after a stroke. Patients may have a history of high blood pressure, vascular disease, or previous strokes or heart attacks. Vascular dementia may or may not get worse with time, depending on whether the person has additional strokes. In some cases, symptoms may get better with time. Nutritional strategies, including antioxidant and flavonoid supplementation may help to maintain a healthy blood flow to the brain and in the entire body in general.
Lewy Body Dementia (LBD) or Dementia with Lewy Bodies is one of the most common types of progressive dementia, which has similarities with Parkinson's and Alzheimer's disease. LBD usually occurs sporadically, in people with no known family history of the disease. In LBD, cells die in the brain's cortex (outer layer), and in a part of the mid-brain called the substantia nigra. Many of the remaining nerve cells in the substantia nigra contain abnormal structures called Lewy bodies that are the hallmark of the disease. Lewy bodies may also appear in the brain's cortex. The symptoms of LBD overlap with Alzheimer's in many ways, and may include memory impairment, poor judgment, and confusion. However, LBD typically also includes visual hallucinations, parkinsonian symptoms such as a shuffling gait and flexed posture, and day-to-day fluctuations in the severity of symptoms. Patients with LBD live an average of 7 years after symptoms begin. There is no cure for LBD, and treatments aim to control the parkinsonian and psychiatric symptoms of the disorder. Patients sometimes respond dramatically to treatment with antiparkinsonian drugs and/or cholinesterase inhibitors, such as those used for AD. Lewy bodies are often found in the brains of people with Parkinson's and Alzheimer's suggesting that either LBD is related to these other causes of dementia or that the diseases sometimes coexist in the same person.
Frontotemporal Dementia (FTD) is a term for a diverse group of relatively uncommon disorders that primarily affect the frontal and temporal lobes of the brain. Experts believe FTD accounts for 2 to 10 percent of all cases of dementia. This group of diseases is characterized by degeneration of nerve cells in the frontal and temporal lobes of the brain. Unlike Alzheimer's, FTD usually does not include formation of amyloid plaques. In many people with FTD, there is an abnormal form of tau protein in the brain, which accumulates into neurofibrillary tangles. This disrupts normal cell activities and may cause the cells to die. Symptoms of FTD usually appear between the ages of 40 and 65. In many cases, people with FTD have a family history of dementia, suggesting that there is a strong genetic factor in the disease. The duration of FTD varies, with some patients declining rapidly over 2 to 3 years and others showing only minimal changes for many years. People with FTD live with the disease for an average of 5 to 10 years after diagnosis.
Huntington's Disease (HD) is a genetic neurological disorder characterized after onset by uncoordinated, jerky body movements and a decline in mental abilities. The faulty gene codes for a protein called huntingtin. The children of people with HD have a 50 percent chance of inheriting it. The disease causes degeneration in many regions of the brain and spinal cord. Symptoms of HD usually begin when patients are in their thirties or forties, and the average life expectancy after diagnosis is about 15 years. Cognitive symptoms of HD typically begin with mild personality changes, such as irritability, anxiety, and depression, and progress to severe dementia. Many patients also show psychotic behavior.
Creutzfeldt-Jakob Disease (CJD) is a very rare, degenerative, fatal brain disorder that affects about one in a million people per year worldwide. Symptoms usually begin after age 60 and most patients die within 1 year. Many researchers believe CJD results from an abnormal form of a protein called a prion. Most cases of CJD occur sporadically - that is, in people who have no known risk factors for the disease. However, about 5 to 10 percent of cases of CJD in the United States are hereditary, caused by a mutation in the gene for the prion protein. In rare cases, CJD can also be acquired through exposure to diseased brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious. Patients with CJD may initially experience problems with muscular coordination; personality changes, including impaired memory, judgment, and thinking; and impaired vision. Other symptoms may include insomnia and depression. As the illness progresses, mental impairment becomes severe. They eventually lose the ability to move and speak, and go into a coma. Pneumonia and other infections often occur in these patients and can lead to death. CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Spongiform refers to the characteristic appearance of infected brains, which become filled with holes until they resemble sponges when viewed under a microscope. In recent years, a new type of CJD, called variant CJD (vCJD), has been found in Great Britain and several other European countries. The initial symptoms of vCJD are different from those of classic CJD and the disorder typically occurs in younger patients. Research suggests that vCJD may have resulted from human consumption of beef from cattle with a TSE disease called bovine spongiform encephalopathy (BSE), also known as "mad cow disease."
Treatments to reverse or halt disease progression are not available for most of the dementias, patients can benefit to some extent from treatment with available medications and other measures, such as cognitive training and nutritional interventions.
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Knowledge Links:
MedlinePlus:
Dementia
Lewy Body Disease
Creutzfeldt-Jakob
Disease
Huntington's disease
Other good dementia websites:
NINDS on Dementias
NINDS on Multi-Infarct Dementia
NINDS on Lewy Body Dementia
NINDS on Huntington's Disease
NINDS on CJD
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