10 types of dementia ;
VIDEO AND ARTICLE:
Dementia is a group of common symptoms over 50 disorders. Alzheimer’s disease is the most common type of dementia. More information on the 10 most common types of dementia.
Dementia is not a specific disease. It is a descriptive term for a set of symptoms that can be caused by a number of disorders that affect the brain. People with dementia have significantly impaired intellectual functioning that interferes with normal activities and relationships. They also lose their ability to solve problems and maintain emotional control, and may experience personality changes and behavioral problems such as agitation, delusions and hallucinations. While memory loss is a common symptom of dementia, memory loss by itself does not mean that a person has dementia. Doctors diagnose dementia only if two or more brain functions – such as memory, language skills, perception, or cognitive abilities, including reasoning and judgment -. Affected significantly without loss of consciousness
Alzheimer’s disease (AD) is the most common cause of dementia in people over 65 years. Experts believe that up to 4 million people in the United States are currently living with the disease: one in ten people over 65 and nearly half of those over 85 have AD. At least 360,000 Americans are diagnosed with AD each year and about 50,000 are reported to die from it.
In most people, symptoms of AD appear after age 60. However, there are some forms of early onset of the disease, usually related to a specific genetic defect, which can appear as early as age 30. AD usually causes a gradual decline in cognitive abilities, usually for a period of 7 to 10 years. Nearly all brain functions, including memory, movement, language, judgment, behavior and abstract thinking, are eventually affected
AD is characterized by two abnormalities in the brain :. Amyloid plaques and neurofibrillary tangles. Amyloid plaques, found in the tissue between the nerve cells, are unusual groups of a protein called amyloid beta bits with degeneration of neurons and other cells.
Tangles are braided tows found inside neurons. These tangles are largely made up of a protein called tau. In healthy neurons, tau protein helps the functioning of microtubules, which are part of the structural support of the cell and deliver substances across the nerve cell. However, in AD tau it is changed in a way that makes twisting in pairs of helical filaments that collect in tangles. When this happens, the microtubules can not function properly and disintegrate. This collapse of the transport system of the neuron may impair communication between nerve cells and cause their death.
Researchers do not know whether amyloid plaques and neurofibrillary tangles are harmful or whether they are merely secondary disease process that damages neurons effects and leads to symptoms of AD. They know that plaques and tangles usually increase in the brain as AD progresses.
In the early stages of AD, patients may experience memory impairment, lapses of judgment and subtle changes in personality. As the disease progresses, memory and language problems worsen and patients begin to have difficulty performing daily activities such as balancing a checkbook or remembering to take medications life. They may also have space, such as difficulty navigating in an unfamiliar route visual problems. They may become disoriented about places and times, can suffer delusions (like the idea that someone is stealing from them or that your spouse is cheating), and can be tempered and hostile. During the later stages of the disease, patients begin to lose the ability to control motor functions. They may have difficulty swallowing and lose bowel and bladder control. Eventually they lose the ability to recognize family members and talk. As AD progresses, it begins to affect emotions and behavior of the person. Most people with AD eventually develop symptoms such as aggression, agitation, depression, insomnia, or delusions.
On average, AD patients live from 8 to 10 years after being diagnosed. However, some people live up to 20 years. AD patients often die of aspiration pneumonia as they lose the ability to swallow late in the course of the disease.
chronic traumatic encephalopathy (CTE) is a progressive degenerative brain disease
CTE was found more frequently in professional athletes involved in football, ice hockey, wrestling and other contact sports that have experienced repetitive brain trauma . It has also been found in soldiers exposed to an explosion or injury of shock, in both cases resulting in the characteristic degeneration of brain tissue and accumulation of an abnormal protein called tau .
still Sorry no less serious injuries bruises and concussions ( “sub-shocks brain”) incurred during play contact sports for a long period repeated to yield CTE. In the case of injury outbreak, a single exposure to an explosion and subsequent violent movement of the head from the blast of wind can cause the disease.
Symptoms of neurodegeneration may occur months, years or even decades after the last brain trauma or end of the active participation of athletics. The degeneration of the brain associated with memory loss, confusion, impaired judgment, problems with impulse control, aggression, depression and eventually progressive dementia.
CCMA has a variant called pugilistic dementia (Pugil means boxer in Latin) or syndrome boxer since head trauma is commonly experienced by people who have been punched many times in the head during boxing.
the most common symptoms of the disease are dementia and parkinsonism, which can occur many years after the trauma ends. Affected individuals may also develop poor coordination and slurred speech.
A single traumatic brain injury can also lead to a condition known as posttraumatic dementia (PTD) . PTD is similar to dementia pugilistica, but usually also includes memory problems long term. Other symptoms vary depending on which part of the brain was damaged by the injury.
corticobasal degeneration (CBD) is a progressive disorder characterized by nerve cell loss and atrophy in multiple areas of the brain. Brain cells of people with CBD often have abnormal accumulations of tau protein. CBD usually progresses gradually over the course of six to eight years. Initial symptoms, which usually start at or around age 60, may appear first on one side of the body, but over time will affect both sides. Some symptoms, such as poor coordination and rigidity, are similar to those found in Parkinson’s disease. Other symptoms may include memory loss, dementia, visual and spatial problems, apraxia (loss of the ability to make familiar movements), confused and hesitant speech, myoclonus (involuntary muscle jerks), and dysphagia (difficulty swallowing). Death is often caused by pneumonia or other secondary problems such as sepsis (serious blood infection) or pulmonary embolism (a blood clot in the lungs).
There are no specific treatments available for CBD. Drugs such as clonazepam can help with myoclonus, however, and occupational, physical and speech therapy can help in managing disability associated with the disease. Symptoms of the disease often do not respond to Parkinson drugs or other drugs.
Creutzfeldt-Jakob disease (CJD) is a rare, fatal brain disorder that affects approximately disorder, degenerative and one of every 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 with 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 through the air or by casual contact with a CJD
Patients with CJD patient may initially experience problems with muscular coordination .; personality changes, including impaired memory, judgment, and thinking; and vision problems. Other symptoms may include insomnia and depression. As the disease progresses, mental impairment becomes severe. Patients often develop myoclonus and can go blind. Eventually they lose the ability to move and talk, and go into a coma. Pneumonia and other infections often occur in these patients and can lead to death.
CJD belongs to a family known as transmissible spongiform encephalopathies (TSEs) human and animal diseases. Spongiform refers to the characteristic appearance of infected brains, which are filled with holes until they resemble sponges when viewed under a microscope. CJD is the most common of the known human TSEs. Others include fatal familial insomnia and Gerstmann-Straussler-Scheinker (see below).
In recent years, a new type of CJD, called variant CJD (vCJD), has been found in Britain and several other European countries. The first symptoms of vCJD are different from those of classical CJD and the disorder typically occurs in younger patients. Research suggests that vCJD may result from human consumption of meat from cattle with a TSE disease called bovine spongiform encephalopathy (BSE), also known as “mad cow disease.”
The frontotemporal dementia (FTD), sometimes called frontal lobe dementia describes a group of diseases characterized by degeneration of nerve cells diseases – especially in the frontal and temporal lobes of the brain. Unlike AD, FTD usually does not include the formation of amyloid plaques. In many people with FTD it is not an abnormal form of tau protein in the brain, which accumulates in neurofibrillary tangles. This alters the normal activity of cells and can cause the cells to die.
Experts believe FTD accounts for 2 to 10 percent of all cases of dementia. 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 two to three 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.
Because structures found in the frontal and temporal lobes of the control statement brain and social behavior, people with FTD often have problems maintaining interactions normal and following social conventions. They may steal or exhibit impolite and socially unacceptable behavior, and they may neglect their normal responsibilities. Other common symptoms include loss of speech and language, compulsive or repetitive behavior, increased appetite, and motor problems such as stiffness and balance problems. Memory loss can also occur, although it typically appears at the end of the disease.
In one type of FTD called Pick’s disease, certain nerve cells become abnormal and swollen before they die. These swells or fired, neurons are a feature of the disease. The brains of people with Pick’s disease also have structures called Pick bodies, largely composed of tau protein within neurons. The cause of Pick’s disease is unknown, but runs in families and therefore is probably due at least in part to a defective gene or genes. The disease usually begins after age 50 and causes changes in personality and behavior that gradually worsen over time. Symptoms of Pick’s disease are very similar to those of AD, and may include inappropriate social behavior, loss of mental flexibility, language problems and difficulty with thinking and concentration. Currently there is no way to slow the progressive degeneration found in Pick’s disease. However, medication may be useful to reduce the aggressiveness and other behavioral problems, and in the treatment of depression.
In some cases, familial FTD is linked to a mutation in the tau gene. This condition, called frontotemporal dementia linked to chromosome 17 (FTDP-17) Parkinsonism, is very similar to other types of FTD but often includes psychiatric symptoms such as delusions and hallucinations.
According to the Mayo Clinic, “Primary progressive aphasia (uh-FAY-zhuh) impairs the ability of language. people with primary progressive aphasia may have trouble expressing their thoughts and understanding or finding words.
PPA can start in people and in their forties. “aphasia” is a general term used to refer to deficits in language functions, such as speaking, understanding what others say, and name common objects.
(primary progressive aphasia is classified by the Mayo Clinic as a type of frontotemporal degeneration , a group of related disorders that originate in the frontal or temporal lobes of the brain. despite its clinical and pathological overlap with FTD , M.-Marsel Mesulam in 1982 described it as a distinct syndrome.)
symptoms usually start gradually progress slowly over a period of years. As the disease progresses, memory and attention may also be affected, patients can show changes in personality and behavior. Many, but not all, people with PPA eventually develop symptoms of dementia.
primary progressive aphasia has three types, which produce different symptoms.
symptoms may vary depending on the situation of speech and the type of primary progressive aphasia. For example, a person may need to pause often to find words during a conversation that requires a high level of accuracy, but then no breaks in the exchange of small talk. Reading and writing often also be affected.
British family Dementia, Danish dementia family, fatal familial insomnia and Gerstmann-Straussler-Scheinker (GSS) are rare hereditary dementias. Symptoms of GSS typically include ataxia and progressive dementia that starts when people are between 50 and 60 years old. The disease can take several years before patients eventually die. Fatal familial insomnia causes degeneration of the brain called the thalamus region, which is partially responsible for controlling sleep. Causes a progressive insomnia that eventually leads to a complete inability to sleep. Other symptoms may include decreased reflexes, dementia, hallucinations, coma and finally. It can be fatal within 7-13 months after symptoms start, but can last longer. British family dementia and familial Danish dementia have been linked to two different defects in a gene on chromosome 13. They found the symptoms of both diseases include progressive dementia, paralysis and loss of balance.
results dementia (HAD) associated with HIV from infection with the human immunodeficiency virus (HIV) that causes AIDS. HAD can cause widespread destruction of the white matter of the brain. This leads to a type of dementia that generally includes impaired memory, apathy, social isolation, and difficulty concentrating. People often had to develop movement problems too. There is no specific treatment for HAD, but AIDS drugs can delay the onset of the disease and may help reduce symptoms.
Huntington’s disease (HD) is an inherited disorder caused by a defective gene for a protein called huntingtin. The children of people with this disorder have a 50 percent chance of inheriting it. The disease causes degeneration in many brain regions and spinal cord. Symptoms of HD usually begin when patients are in their thirties or forties, and the average life expectancy after diagnosis is 15 years.
The cognitive symptoms of HD typically begin with mild personality changes, such as irritability, anxiety and depression, and severe dementia progress. Many patients also show psychotic behavior. HD causes chorea – jerky involuntary movements, arrhythmic body -., As well as muscle weakness, clumsiness and gait disturbances
Lewy body dementia (LBD) is one of the most common types of progressive dementia. Symptoms of dementia with Lewy bodies overlap with those of other diseases, so it is difficult to diagnose.
LBD usually occurs sporadically, in people with a known family history of the disease. However, occasionally they have been reported rare familial cases.
Lewy body dementia, involving protein aggregates called Lewy bodies, balloon-like structures formed within nerve cells. Initial symptoms may vary, but over time, people with these disorders develop cognitive, behavioral, physical and related symptoms very similar dream. Lewy body dementia is one of the most common causes of dementia, after Alzheimer’s disease and vascular disease. Dementias with Lewy bodies include:
Dementia with Lewy bodies (DLB) , one of the most common forms of progressive dementia. Symptoms such as difficulty sleeping, loss of smell, and visual hallucinations often precede movement and other problems for up to 10 years, which consequently results in the DCL go unrecognized or misdiagnosed as a psychiatric disorder until his last stages. The neurons of the substantia nigra that produce dopamine die or become impaired, and the outer layer of the brain (cortex) degenerates. Many remaining neurons contain Lewy bodies.
Later in the course of DCL, some signs and symptoms are similar to AD 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, shuffling walk, and changes in alertness and attention. Given these similarities, DLB can be very difficult to diagnose. There is no cure for DLB, but there are drugs that control some of the symptoms. The medications used to control symptoms of DCL can worsen motor function or exacerbate hallucinations.
dementia of Parkinson’s disease (PDD) , a clinical diagnosis related to DCL it can occur in people with Parkinson’s disease. PDD can affect memory, social judgment, language, or reasoning. Autopsy studies show that people with TGD often have amyloid plaques and tau tangle similar to those found in people with AD, although it is not clear what these similarities. A majority of people with Parkinson’s disease develop dementia, but the time of onset of symptoms of movement to the onset of symptoms of dementia varies greatly from person to person. Risk factors for the development of PDD include the appearance of symptoms related movement with Parkinson’s followed by disorder of decay and REM mild cognitive behavioral sleep, which involves having frequent nightmares and visual hallucinations.
vascular dementia is the second most common cause of dementia, after year. It is responsible for up to 20 percent of all dementias and is caused by brain damage due to stroke or cardiovascular problems – usually strokes. It can also result from genetic diseases, endocarditis (infection of a heart valve), or amyloid angiopathy (a process in which amyloid protein accumulates in the blood vessels of the brain, sometimes causing hemorrhagic or “bleeding” strokes). In many cases, it can coexist with AD. The incidence of vascular dementia increases with age and is similar in men and women.
Symptoms of vascular dementia often begin suddenly, often after a stroke. Patients may have a history of high blood pressure, vascular disease or previous stroke or heart attacks. Vascular dementia may or may not get worse over time, depending on whether the person has additional strokes. In some cases, symptoms may improve over time. When the disease does not worsen, often progresses in a stepwise manner, with sudden changes in capacity. Vascular dementia with brain damage midbrain regions, however, can cause progressive cognitive impairment, progressive may seem very similar to AD. Unlike people with AD, people with vascular dementia often maintain their personality and normal levels of emotional responsiveness until the later stages of the disease.
People with vascular dementia frequently wander at night and often have other problems commonly found in people who have had a stroke, including depression and incontinence.
There are several types of vascular dementia, which vary slightly in their causes and symptoms.
One type of vascular dementia is called multi-infarct dementia (MID) . It is caused by numerous small strokes in the brain. MID typically includes multiple damaged areas, called infarctions, plus extensive lesions in the white matter, or nerve fibers of the brain.
Because the infarcts in MID affect isolated areas of the brain, the symptoms are usually limited to one side of the body or may affect only one or a few specific areas, such as language functions. Neurologists call unlike “global” symptoms seen in AD, which affect many functions and are not restricted to one side of the body to these “local” or “focal” symptoms.
This article was originally published on alzheimersweekly, Read the original article here