|MRI-like test plan for Alzheimer’s|
|New Delhi, April 9: Medical researchers in India have proposed what they say could be a non-invasive test for the early detection of Alzheimer’s disease and mild cognitive impairment, a condition that always precedes this incurable degenerative brain disorder.Their study has shown for the first time that a test similar to a magnetic resonance imaging (MRI) scan may be used to measure the levels of a key brain chemical believed to be associated with cognitive, or intellectual, impairment and Alzheimer’s disease.
Researchers at the National Brain Research Centre in Manesar, Haryana, have demonstrated through studies on patients and healthy people that the chemical glutathione is steadily depleted as the degree of cognitive impairment grows.
“The lower the glutathione levels, the greater the cognitive deterioration,” Pravat Mandal, the professor who led the study, told The Telegraph. The findings have been accepted by the international journal Biological Psychiatry.
“We found that patients with Alzheimer’s disease had the lowest levels of glutathione,” Mandal said.
Glutathione, produced by brain cells, is what scientists call an “anti-oxidant”. It protects biological tissues from a destructive process called oxidation stress.
Over the past decade, several independent research groups in Europe and North America have found indirect evidence that depleted glutathione levels may increase oxidative stress in the brain and contribute to the sequence that leads to Alzheimer’s.
But until now, no studies on living human patients had established any direct link between glutathione and cognitive impairment or Alzheimer’s. Standard clinical diagnosis involves behaviour assessment, MRI scans to examine changes in the brain, and cerebro-spinal fluid analysis.
Mandal and his colleagues used a technique called magnetic resonance spectroscopy to measure glutathione in two regions of the brain – the hippocampus and the frontal cortex – of patients diagnosed with mild cognitive impairment or Alzheimer’s disease, and a set of healthy people.
Their study found that specific glutathione levels in both the hippocampus and the frontal cortex appeared sharply correlated with the degree of cognitive impairment. Glutathione in other areas of the brain appeared unchanged between patients and healthy people.
“This opens up some exciting possibilities for the future, for diagnosis and therapy,” said Manjari Tripathi, a professor of neurology at AIIMS who had collaborated with the Manesar researchers.
Several common foods, including broccoli, cabbage, onion, garlic and turmeric, are rich in glutathione and, Tripathi said, it may be a good idea to examine how long-term and steady consumption of such foods could impact glutathione levels in the brain. Only tiny quantities of glutathione consumed through food would reach the brain.
“So what this means is a long-term, lifestyle-based consumption of glutathione-rich foods,” Tripathi said.
However, the researchers have cautioned that while their study strongly suggests that glutathione is “intricately tied” to the biological processes that lead to Alzheimer’s, the precise cause of the glutathione depletion remains unclear.
Neurologists distinguish between mild cognitive impairment and dementia, or Alzheimer’s, depending on the number of symptoms patients display.
Updates on Alzheimer’s/ Dementia Research
Novel Way to Treat Alzheimer’s
The blood-brain barrier has posed one of the biggest challenges in treating Alzheimer’s disease. Now, researchers have been able to overcome this hurdle. In a paper published on March 11 in the journal Science Translation Medicine, a team led by Jurgen Gotz of Queensland Brain Institute. Australia, was able to send a drug across the blood-brain barrier using a combination of microbubbles and ultrasound waves. They tested the method on mice.
Alzheimer’s disease involves plaques of beta-amy-loid forming in the brain. Cells that would normally eat up such deposits fail to do so in an affected person.
Normally, such a feature would be treated by sending drugs through the blood stream. In the case of AD this is not possible because of what is known as the blood-brain barrier. This is a group of closely packed cells that normally protect the brain. It also makes the brain difficult to treat by normal procedures.
Discovered: Key to blocking Alzheimer’s progress
A molecule that can block the progress of Alzheimer’s disease at a crucial stage in its development has been identified by British researchers. A molecular chaperone has been found to inhibit a key stage in the development of Alzheimer’s and break a chain reaction that leads to the death of brain cells.
The research provides an effective basis for finding candidate molecules that could be used to treat the condition. Cambridge University scientists have shown that a molecular chaperone, a type of molecule that occurs naturally in humans, can play the role of an “inhibitor” part-way through the process that is thought to cause Alzheimer’s, breaking the cycle of events that scientists believe leads to the disease.
Specifically, the molecule, called Brichos, sticks to threads made up of malfunctioning proteins, called amyloid fibrils. By doing so, it stops these threads from coming into contact with other proteins, thereby helping to avoid formation of highly toxic clusters that enable the condition to proliferate in the brain.
Cracked: Chain of events that leads to Alzheimer’s
Breakthrough Could Cut Time And Cost Of Drug Hunt
Scientists have for the first time replicated the full course of events underlying the development of Alzheimer’s disease inside a lab. A novel 3D culture system replicates the course of Alzheimer’s, which doctors feel could significantly reduce time and cost of drug development.
Researchers from the Massachusetts General Hospital in Boston showed that the deposition of beta-amyloid plaques in the brain is the first step in a cascade leading to the devastating neurodegenerative disease. They also identified the essential role in that process of an enzyme, inhibition of which could be a therapeutic target.
The MGH team used a gel based, 3D culture system to grow human neural stem cells that carried variants in two genes – the amyloid precursor protein and presenilin 1 – known to underlie early-onset Familial Alzheimer’s Disease (FAD). Both the genes were co-discovered in lead researcher Rudolph E Tanzi’s laboratory.
“This new system – which can be adapted to other neurodegenerative disorders – should revolutionize drug discovery in terms of speed, costs and physiologic relevance to disease,” Tanzi said.