Thursday, August 23, 2012

HS-Aging – Looks like Alzheimer’s, but not Alzheimer’s

Many different diseases may produce symptoms of dementia - defined as cognitive decline and impaired memory - in aged persons. Although Alzheimer's disease is probably the most recognized cause of dementia, HS-AGING also causes serious cognitive impairment in older adults. In those who live to a very advanced age (beyond the age of 95) HS-AGING is roughly as prevalent as Alzheimer's.

It is important for physicians and scientists to understand the unique pathology of HS-AGING, and to be able to differentiate it from other diseases, as it is only by making an accurate diagnosis that clinicians can hope to treat people who present with signs of cognitive decline. 

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What is HS-Ageing?

HS-Ageing stands for “Hippocampal Sclerosis in Ageing People”. Both Alzheimer’s and HS-Ageing are different types of dementia. In people aged 65 to 95, 60% of dementia cases are Alzheimer’s. That is why Alzheimer’s is so well-known. At age 95, the balance shifts and HS-Ageing becomes about as common as Alzheimer’s. And when dementia is seen in the elderly, the default diagnosis is Alzheimer's. This is caused by many factors, among them:
  • Patients often do not want to go through extensive testing for a variety of reasons.
  • There is no simple test. The differences between dementias can be subtle. Therefore, distinguishing between dementias is often technically challenging.
  • Cost comes into play. For example, F18 dementia scans can run thousands of dollars. Therefore, many a diagnosis is made based on incomplete information.

With these realities, it is common for a diagnosis to default to the most common dementia, which is Alzheimer's. As a result, people with dementias such as HS-Ageing often live out their lives thinking they have Alzheimer's.
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How does HS-Ageing differ from Alzheimer’s?

Alzheimer’s and HS-Ageing both damage the hippocampus. It seems that HS-Ageing hits harder than Alzheimer’s, causing greater disturbances to memory.

HS-Ageing puts a brain under attack from a protein called TDP-43. It causes sclerosis, or the hardening of tissues. In the case of HS-Ageing, TDP-43 proteins harden brain tissue in the hippocampus (sometimes called the memory-processing center), causing the loss of a large number of crucial brain cells. It is called Hippocampal Sclerosis because the brain’s hippocampus is the focus of the attack.

Alzheimer’s, on the other hand, is an attack on the brain by plaques (made from beta-amyloid) and tangles (made of tau proteins). Researchers speculate that the plaques clump together and “choke” brain cells, while the tangles strangle them from within.

How does HS-Ageing differ from regular HS?

Regular Hippocampal Sclerosis (HS) occurs in younger people where brain tissue hardening is associated with epilepsy. HS-Ageing is a similar hardening, but it occurs in the elderly with different consequences. It is caused by a long life of physical wear-and-tear on the brain, similar to vascular dementia. As a matter of fact, once people hit 95, the combined occurrence of HS-Ageing PLUS vascular dementia actually outstrip Alzheimer’s.

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Why does the type of dementia matter?

As explained above, the biochemistry of each dementia differs significantly. This implies different medications are required to fight the chemicals causing the dementia. A person’s response to medicines and supplements will be entirely different, depending on the disease.

Importantly, new F18 imaging techniques have recently been introduced that let doctors see if a person with dementia has the plaques associated with Alzheimer's. Using this technique helps doctors tell the difference between Alzheimer’s and HS-Ageing. This is particularly crucial in the world of clinical trials, where participants must closely match the experimental drugs they are testing.

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It is important for physicians and scientists to understand the unique pathology of HS-AGING, and to be able to differentiate it from other diseases, as it is only by making an accurate diagnosis that clinicians can hope to treat people who present with signs of cognitive decline.

Nelson, a neuropathologist, analyzed autopsy data from 1,100 individuals (2011), each with substantial clinical data available from before death. The long-term clinical information was obtained through the University of Kentucky Alzheimer's Disease Center, the Nun Study and the Georgia Centenarian Study (all autopsies were performed at the University of Kentucky). The large numbers of patients and the high quality of the data enabled the research team to gather new clues about the prevalence and impact of HS-AGING.

"We and others have shown previously that HS-AGING has a strong impact on cognition. The goal of the new study was to define HS-AGING as a distinct disease entity," said Nelson.

"There were some surprises. The high prevalence of HS-AGING in individuals older than 95 was unexpected. In addition, by analyzing neuropathological data alongside clinical data, we were able to determine that there is a recognizable cognitive profile for individuals likely to develop HS-AGING," said Nelson.

In the future, clinicians may be able to utilize cognitive tests with increased accuracy to differentiate a diagnosis of HS-AGING from a general diagnosis of cognitive decline. Being able to pinpoint the cause of cognitive decline may lead to better and more accurate diagnosis and treatment of aging individuals who present with signs of dementia.

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