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The deactivation of two genes could be the cause of Alzheimer's
June 01, 2004Alzheimer's disease could be caused by the deactivation of what are known as "presenilin genes". Using mice as a model for the study of Alzheimer's in humans, a scientific team headed by the researcher Carlos Saura, from the Universitat Autònoma de Barcelona, has discovered that when these genes mutate and stop working they cause neuro-degeneration and memory loss, giving rise to what in humans would be Alzheimer's. The discovery, published in Neuron, is totally unexpected, since up till now it was thought that the alteration that caused Alzheimer's was exactly the opposite, that is to say, an excess of presenilin activity.
Since 1995 it has been known that family hereditary Alzheimer's is caused mainly by mutations in presenilin genes, but it was thought that the alteration of these genes caused Alzheimer's due to an increase in their activity. Research by doctor Carlos Saura, of the Neuroscientific Institute (l'Institut de Neurocie'ncies (IN)) at the Universitat Autònoma de Barcelona, using mice, genetically modified to decrease the activity of presenilin genes, has shown that these genes take part in the process of memory consolidation and neuron survival, but in a different way to that expected.
The results, published in the journal Neuron last April, show that the absence of activity of these genes in mice, used as a model for the study of Alzheimer's in humans, causes symptoms very similar to those observed in persons suffering from Alzheimer's: progressive memory loss and neuro-degeneration. The authors suggest that mutations in presenilins could be a cause of Alzheimer's, mainly due to loss of functionality.
Besides, in this study the researchers identify the molecular mechanisms by which the deactivation of these genes in the mice's brains leads to memory loss and neuron death. According to this study, the presenilins regulate a group of genes that take part in the process of memory formation. The study suggests that in the first stages of the illness there is a decline in presenilin activity which leads to an imbalance in the cellular processes that control memory and causes neuron death.
The discovery opens new avenues for treatment and prevention of Alzheimer's disease, a neuro-degenerative disease that affects 400,000 people in Spain, and without any effective treatment. In the opinion of doctor Carlos Saura "pharmacological treatment that activates the cellular pathways regulated by presenilins could prevent or improve memory loss in patients".
Barcelona, Universitat Autònoma de
Besides, in this study the researchers identify the molecular mechanisms by which the deactivation of these genes in the mice's brains leads to memory loss and neuron death. According to this study, the presenilins regulate a group of genes that take part in the process of memory formation. The study suggests that in the first stages of the illness there is a decline in presenilin activity which leads to an imbalance in the cellular processes that control memory and causes neuron death.
The discovery opens new avenues for treatment and prevention of Alzheimer's disease, a neuro-degenerative disease that affects 400,000 people in Spain, and without any effective treatment. In the opinion of doctor Carlos Saura "pharmacological treatment that activates the cellular pathways regulated by presenilins could prevent or improve memory loss in patients".
Barcelona, Universitat Autònoma de
Alzheimer Disease Current Events and Alzheimer Disease News RSSDelirium in hospitalized adults: Situation critical, no relief available
Every year as many as seven million adults in the United States experience delirium during hospitalization.
New data demonstrate potential for early detection of Alzheimer's disease
Data published in the June issue of the Journal of Alzheimer's Disease demonstrated that minimally-invasive biospectroscopy was able to identify changes in oxidative stress (OS) levels in blood plasma, which may prove to be a useful biomarker in the early detection of Alzheimer's disease.
Another McGill/JGH breakthrough opens door to early Alzheimer's diagnosis
A new diagnostic technique which may greatly simplify the detection of Alzheimer's disease has been discovered by researchers at McGill University and the affiliated Lady Davis Institute for Medical Research at Montreal's Jewish General Hospital (JGH).
Measuring brain atrophy in patients with mild cognitive impairment
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Commonly used medications may produce cognitive impairment in older adults
Many drugs commonly prescribed to older adults for a variety of common medical conditions including allergies, hypertension, asthma, and cardiovascular disease appear to negatively affect the aging brain causing immediate but possibly reversible cognitive impairment, including delirium, in older adults.
Commonly used ulcer drugs may offer treatment potential in Alzheimer's disease
In a new study, published in the May issue of Elsevier's Experimental Neurology, scientists at the University of British Columbia have discovered that drugs commonly used to treat ulcers have significant neuroprotective properties, which appear to be enhanced when used in combination with ibuprofen, a widely used anti-inflammatory drug.
New test for mysterious metabolic diseases developed at Stanford/Packard
Scientists at Stanford University School of Medicine have devised a much-needed way to monitor and find treatments for a mysterious and devastating group of metabolic diseases that arise from mutations in cells' fuel-burning mechanism.
Recalibrating 'fight or flight'
A Canadian/U.S. research team has reported a novel approach to stimulating recovery from chronic stress disorders. Details of the therapeutic model, which exploits the natural dynamics of the body's "fight or flight" system, are published January 23 in the open-access journal PLoS Computational Biology
Vitamin B does not slow cognitive decline in Alzheimer's
A clinical trial led by Paul S. Aisen, M.D., professor of neurosciences at the University of California, San Diego School of Medicine, showed that high-dose vitamin B supplements did not slow the rate of cognitive decline in patients with mild to moderate Alzheimer disease.
Protecting patient privacy the new fashioned way
Protecting patient privacy has been recognized as the duty of health-care providers for about as long as doctors have seen patients. In 1996 that duty became a legal obligation when Congress passed the Health Insurance Portability and Accountability Act.
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