Site updated at Wednesday, 22 June 2016

Living with Dementia

Q: A person can die of Alzheimer’s? I thought it was just an extreme case of senility!

A: It’s more than that, although dementiaa condition that many people refer to as senilityis its most prominent characteristic.

Alzheimer’s disease actually destroys brain cells. As the disease progresses, more brain cellsand more abilitiesare lost. In its final stages, Alzheimer’s disease affects a person’s ability to control movement, bowel and bladder and his ability to communicateleaving him completely dependent upon others, susceptible to a host of ailments and unable to recognize and seek help for his symptoms.

Q: But some amount of intellectual decline is normal in old age, isn’t it? Just how does dementia differ from normal aging?

A: It is true that many older people experience a minor degree of forgetfulness (known as benign senescent forgetfulness) as well as a slowing of physical and mental agility. In fact, the term senile, which many people use to mean ‘‘forgetful,” is actually defined as “relating to old age.”

But the forgetfulness and mental slowing that occur with age generally do not interfere with daily life; they are not disabling. Dementia, by definition, involves intellectual declines or losses severe enough to…

Have a Question !

Dementia - Living with dementia

Pick's disease and the frontal dementias

Dementias believed to be related to frontal lobe pathology have once again become of interest, and authors often invoke the name of Arnold Pick (Niery et al., 1988). However, when the great Prague neuropsychiatrist described the syndrome named after him, all he wanted was to draw attention to a form of localized (as opposed to diffuse) atrophy of the temporal lobe (Pick, 1892). This alteration was to give rise to a dysfunction of language and praxis, and be susceptible to diagnosis during life. Pick believed that lobar atrophies constituted a stage in the evolution of the senile dementias.

The story starts, as it should, before Pick. Louis Pierre Gratiolet (1854) was responsible for renaming the cerebral lobes after their overlying skull: thus 'anterior' became 'frontal' lobe. He made no assumption as to the function of the 'anterior extremity of the cerebral hemisphere'. 'Phrenologists', however, did and related reflective and perceptive functions (qualitatively defined) to the forehead (Anonymous, 1832) (for the science of phrenology see Combe, 1873; Lanteri-Laura, 1970). 'Modular' assumptions (i.e. a one-to-one correlation between mental function and brain site) involving the frontal lobes started only during the 1860s, following reports on dysfunction of language in lesions of the frontal lobes (Broca, 1861; Henderson, 1986). These claims ran parallel to those of Jackson's that the cerebral cortex was the general seat of personality and mind (Jackson, 1894). Meynert (1885) believed that 'the frontal lobes reach a high state of development in man' but still defined mental disorders as diseases of the 'fore-brain' (by which he meant 'prosencephalon' or human brain as a whole).... read more »

Huntington's Disease

Huntington's Disease (Huntington's Chorea)

Huntington's Disease (HD) is a brain disorder that affects a person's ability to think, talk, and move.

The disease destroys cells in the basal ganglia, the part of the brain that controls movement, emotion, and cognitive ability. HD is caused by a mutation in a gene on chromosome 4. The job of its protein product, huntingtin, is to direct the delivery of small packages (vesicles containing important molecules) to the outside of the cell. Normally, the coding region of this gene contains the DNA sequence "CAG" repeated again and again. The number of times this triplet is repeated varies from person to person, ranging from 10 to 26 times. People with HD have an abnormally high number of these CAG triplets, approximately 40 or more. This likely disrupts the function of the gene's protein product, but how the expansion of the CAG repeat causes disease is unknown. Somehow the brain cells of HD patients accumulate clumps of protein that become toxic, resulting in cell death. Some patients lose more than 25% of their brain cells before they die.

How do people get Huntington's Disease?
Huntington's disease is inherited in an autosomal dominant pattern. This means that everyone who inherits the faulty gene will eventually get the disease. A parent with a mutation in the HD gene has a 50 percent chance of passing on the disease to their children.

Huntington's disease symptoms include:
  • Involuntary movements
  • Psychiatric symptoms such as depression, anxiety and psychosis
  • Gait abnormalities with falling
  • Cognitive decline (dementia)

Patients with Huntington's disease possess a different gene than those without it. Neurologists at Emory are now able to predict if an at-risk patient will develop Huntington's disease. Huntington's disease is a genetic disorder caused by a mutation in the gene huntingtin. The gene is inherited in an autosomal dominant fashion, which means that children of a person with Huntington's disease have a 50% chance of inheriting it. Every patient who inherits the gene ultimately develops the disease. ... read more »

Alzheimer’s Disease

prevention of delirium1 - induced pluripotent stem cells1 - tau3 - dementia alliance1 - dopamine levels1 - magnetic resonance imaging3 - ad prognosis1 - genomic dna1 - paraphrenia1 - diabetes10 - schizophrenia1 - alzheimer's causes1 - kahlbaum3 - degenerative neurological disorder1 - rigidity1 - brain insulin1 - symptoms of alzheimer's2 - familial alzheimer's disease2 - alzheimer's patients7 - voxel-based morphometry1 - dementia parkinson's disease1 - beta-amyloid protein1 - alzheimer's proteins1 - problems with language1 - beta amyloid plaques1 - cytokine storm1 - short-term memory problems1 - visual hallucinations1 - risk for cognitive decline1 - social engagement1 -