The following articles have special meaning for me considering that my father spent the last ten years of his life with Alzheimer's disease and I spent most of my twenties dealing with schizophrenia.
CHARLIE FIDELMAN, in The Montreal Gazette, of January 6, 2009 reports of a study warning that Dementia could become epidemic, and that Alzheimer's patients are getting younger.
The Alzheimer Society of Canada is warning that the number of Canadians living with Alzheimer's disease or dementia is expected to swell to epidemic proportions within a generation.
About half a million Canadians - 119,700 of them Quebecers - are affected. The new study, made public yesterday, predicts that within 25 years, the number of cases of Alzheimer's or a related dementia will more than double, ranging between one million and 1.3 million people.
Researchers stress that the findings, presented in a report called Rising Tide: The Impact of Dementia on Canadian Society, should be a clear signal that more effective treatment and preparation is needed in order to avoid a meltdown within the Canadian health care system. The initial findings report the first new prevalence data since the 1991 Canadian Study on Health and Aging.
"These new data only reinforce the fact that Alzheimer's disease and related dementias are a rising concern in this country, an epidemic that has the potential to overwhelm the Canadian health-care system," Ray Congdon of the Alzheimer Society said in a statement.
The most common form of dementia, Alzheimer's, affects one in 11 Canadians over 65. A degenerative disease that slowly destroys memory, reasoning and orientation, Alzheimer's affects how people think, remember and communicate.
But Alzheimer's is not just a disease of the elderly.
The new data suggest an increasing number of baby boomers are also being struck. About 71,000 Canadians under the age of 65 are living with Alzheimer's disease or a related dementia. Approximately 50,000 are 59 or younger. In Quebec, more than 17,140 are under age 65.
"It's urgent we come up with better treatment or there will be an epidemic," said cognitive neurologist Howard Chertkow, a McGill University professor and director of the Bloomfield Centre for Research in Aging at the Jewish General Hospital.
The rising number of cases is no hype, Chertkow said, which explains the push to get the topic on the front burner.
Research suggests Alzheimer's begins about 20 years before symptoms appear, Chertkow said. But despite better awareness and detection tools, there's still a gap between the number of people who are affected by dementia and the number that show up at clinics for evaluation and treatment, he said.
"Some people think it's normal for Grandpa to become senile and lose his memory. So why take a person like that to the doctor?"
There is no cure, but researchers have made progress in understanding the disease, its causes, what makes people susceptible and how it can be prevented.
The report set out to evaluate the economic impact the increasing incidence of the disease will have on the economy. That analysis will be made public when the full report is issued this year.
A provincial working group developing strategies on dementia is expected to complete its report next month.
Dementia causes cognitive impairment, resulting in the loss of memory, attention and reason.
According to en.wikipedia.org, higher mental functions are affected first in the process. Especially in the later stages of the condition, affected persons may be disoriented in time (not knowing what day of the week, day of the month, month, or even what year it is), in place (not knowing where they are), and in person (not knowing who they are or others around them). Symptoms of dementia can be classified as either reversible or irreversible, depending upon the etiology of the disease. Less than 10 percent of cases of dementia are due to causes which may presently be reversed with treatment.
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Alzheimer's/Schizophrenia Link Discovered
ScienceDaily (May 9, 2008) — Neuroscientists at Johns Hopkins have discovered that mice lacking an enzyme that contributes to Alzheimer disease exhibit a number of schizophrenia-like behaviors. The finding raises the possibility that this enzyme may participate in the development of schizophrenia and related psychiatric disorders and therefore may provide a new target for developing therapies.
The BACE1 enzyme, for beta-site amyloid precursor protein cleaving enzyme, generates the amyloid proteins that lead to Alzheimer's disease. The research team years ago suspected that removing BACE1 might prevent Alzheimer.
"We knew at the time that in addition to amyloid precursor protein, BACE1 interacts with other proteins but we didn't know how those interactions might affect behavior," says Alena Savonenko, M.D., Ph.D., an assistant professor in neuropathology at Hopkins.
Reporting in the Proceedings of the National Academies of Sciences, the research team describes how mice lacking the BACE1 enzyme show deficits in social recognition among other behaviors classically linked to schizophrenia.
A normal mouse, when introduced to another mouse, shows a lot of interest the first time they meet. If the mice are separated then reintroduced, their interest drops because they remember having met before, a phenomenon the researchers call habituation. If they then introduce a completely different mouse, interest piques again at the newbie.
The researchers introduced mice lacking BACE1 to another mouse. The first time they met, the BACE1 mouse showed interest, the second time meeting the same mouse the BACE1 mouse showed less interest and even less interest the third time. The researchers then introduced the BACE1 mouse to a totally different mouse of a different strain and the BACE1 mouse showed no interest at all. "These mice were totally disinterested, normal mice just don't behave like this," says Savonenko.
Additionally, the researchers found that these BACE1-lacking mice also displayed many other schizophrenia-like traits. Most importantly, according to Savonenko, some of the deficits improved after treatment with the antipsychotic drug clozapine.
Because schizophrenia is a disorder likely caused by many different factors, Savonenko explains that BACE1 might contribute to an increased risk of schizophrenia in certain patients and the BACE1 mice will be a useful animal model. "We never thought we would see one mouse that closely mimics so many of the clinical features of schizophrenia," says Alena Savonenko, M.D., Ph.D., an assistant professor of neuropathology at Hopkins. "This could be a really useful model to study and understand the molecular contributions to the disease."
The research was funded by the National Institutes of Health, the National Institute on Aging, the Alzheimer's Association, the Adler Foundation, the Ilanna Starr Scholar Fund and the Bristol-Myers Squibb Foundation.
Authors on the paper are Savonenko, T. Melnikova, F. Laird, K.-A. Stewart, D. Price and P. Wong, all of Hopkins.
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