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A new drug designed to prevent the early stages of Alzheimer’s disease could enter clinical trials in a few years’ time, according to scientists.
Christina Mediate's comment,
February 24, 2013 5:56 PM
Being able to stop the formation of senile plaques makes this drug look promising. Those plaques are what cause the damage to the brain cells and start the initial memory loss. I'm anxious to see how it works on humans though. Right now it's only safe on the mice. But this is a very crucial step towards a possible new treatment or cure for the disease.
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Researchers at Mayo Clinic in Florida have uncovered a toxic cellular process by which a protein that maintains the health of neurons becomes deficient and can lead to dementia.
The findings shed new light on the link between culprits implicated in two devastating neurological diseases: Alzheimer’s disease and amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, which afflicts physicist Stephen Hawking. There is no cure for frontotemporal dementia, a disorder that affects personality, behavior and language and is second only to Alzheimer’s disease as the most common form of early-onset dementia.
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Researchers at Johns Hopkins Medicine have surgically implanted a pacemaker-like device into the brain of a patient in the early stages of Alzheimer’s disease, the first such operation in the United States.
The device, which provides deep brain stimulation and has been used in thousands of people with Parkinson’s disease, is seen as a possible means of boosting memory and reversing cognitive decline.
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An efficient, high-volume technique for testing potential drug treatments for Alzheimer's disease uncovered an organic compound that restored motor function and longevity to fruit flies with the disease, according to new research that could help... Via LeapMind
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A new study suggests that physical activity may mitigate cognitive decline in older adults.
Men who were inactive displayed the greatest atrophy (brain shrinkage).
Contrary to common understanding, social and intellectual activity did not appear to affect shrinkage according to this study.
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Researchers compared vitamin E levels in Alzheimer's, mild cognitive impairment, and cognitively normal subjects.
Individuals with cognitive impairment or Alzheimer's had lower blood levels of vitamin E.
The study concluded that both disorders were associated with increased vitamin E damage. Low plasma tocopherols and tocotrienols levels are associated with increased odds of MCI and AD.
Neurobiol Aging. 2012 Oct;33(10):2282-90. Epub 2011 Dec 20.
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The number of U.S. residents aged 65 and older living with Alzheimer's disease is expected to nearly triple to 13.8 million by 2050 as aging baby boomers swell the ranks of those living with the brain-wasting disease, U.S. researchers said on Wednesday.
Greg Wurn's comment,
February 8, 2013 1:40 PM
one of the reason they are feeding flouride to the population, kill them with cancer before they get Alzhimers
Christina Mediate's comment,
February 24, 2013 5:13 PM
I've read that there was hope to have a cure for Alzheimer's by 2025 several times throughout my research. However, this article is saying that the efforts of the Obama Administration to help find this cure, could be unsuccessful due to cutting costs. It's already to late for my grandmother seeing as how she has been living with this disease for about 15 years and is now 86 years old.
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Researchers are investigating the use of pacemaker-like devices for the treatment of Alzheimer’s disease.
Ray and Terry's 's insight:
The process of deep brain stimulation involves using a pacemaker-like implanted device to apply controlled mild electrical pulses to specific areas of the brain. In recent studies, it has been used – with some success – to treat conditions such as Parkinson's disease, major depression and Tourette syndrome. Now, in the ADvance Study, researchers at several research centers are exploring its use in restoring memory function to people with Alzheimer’s disease.
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Earlier this year, researchers identified the intracellular mechanisms regulated by vitamin D3 that may help the body clear the brain of amyloid beta, the main component of plaques associated with Alzheimer's disease.
Published in the March 6 issue of the Journal of Alzheimer's Disease, the early findings show that vitamin D3 may activate key genes and cellular signaling networks to help stimulate the immune system to clear the amyloid-beta protein.
Previous laboratory work by the team demonstrated that specific types of immune cells in Alzheimer's patients may respond to therapy with vitamin D3 and curcumin, a chemical found in turmeric spice, by stimulating the innate immune system to clear amyloid beta. But the researchers didn't know how it worked.
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In neurodegenerative diseases, the choroid plexus and CPECs age prematurely, resulting in reduced CSF formation and decreased ability to flush out the plaque-forming proteins that are a hallmark of Alzheimer’s.
Transplant studies have provided proof of concept for CPEC-based therapies. However, such therapies have been hindered by the inability to expand or generate CPECs in culture.
“Our method is promising, because for the first time we can use stem cells to create large amounts of these epithelial cells, which could be utilized in different ways to treat neurodegenerative diseases,” said Monuki, an associate professor of pathology & laboratory medicine and developmental & cell biology at UCI.
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Mayo Clinic study in seniors finds that diets high in sugars and starches promote brain fog and dementia.
Correlations between carb intake and brain fog included: *Those with the highest carbohydrate intake relative to total fat and protein intake were 3.6 times likelier to develop MCI.
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