here is no cure for Alzheimer’s, the insidious fatal disease which slowly kills all your brain cells. Already the seventh leading cause of death in the US, it is soon to reach epidemic levels as the boomers becomes senior citizens. There are more than 30 million people with dementia worldwide, but by 2050, this figure will increase to over 100 million. Two sets of findings released in the last few days bring hope that the accelerating research effort will find better ways to treat the disease, delay its onset, or prevent it from developing. Most significantly, a simple and inexpensive eye test could aid detection and diagnosis of Alzheimer’s at an earlier stage than is currently possible and a “cocktail” of commonly available supplements has shown promise in improving memory and fighting Alzheimer’s. Alzheimer’s disease was named after German physician Alois Alzheimer, who first described it in 1906. In the subsequent century, we’ve learned a lot about Alzheimer’s but with the ageing of the global population, it is about to become an epidemic. Currently there are more than 30 million people with dementia worldwide. By 2050, this figure will increase to over 100 million. Alzheimer’s is the most common form of dementia, accounting for 50 to 70 percent of dementia cases. It destroys brain cells, causing memory loss and problems with thinking and behavior severe enough to affect work, lifelong hobbies and social life. Alzheimer’s gets worse over time, and keeps destroying brain cells until there are none left. Accordingly, it is inevitably fatal with a mean life expectancy following diagnosis of approximately seven years. Today it is the seventh-leading cause of death in the United States. The most novel concept to come out of the three sets of research published in the last week is from University College London, where researchers have demonstrated a new technique that enables retinal, and therefore brain cell death, to be directly measured in real time. Few people realize that the retina is a direct, albeit thin, extension of the brain. It is entirely possible that in the future a visit to a high-street optician to check on your eyesight will also be a check on the state of your brain.“The death of nerve cells is the key event in all neurodegenerative disorders – but until now it has not been possible to study cell death in real time”, said Professor Cordeiro, of the UCL Institute of Ophthalmology.“This technique means we should be able to directly observe retinal nerve cell death in patients, which has a number of advantages in terms of effective diagnosis.
This could be critically important since identification of the early stages could lead to successful reversal of the disease progression with treatment. Currently, the biggest obstacle to research into new treatments for neurodegenerative diseases is the lack of a technique where the brain’s response to new treatments can be directly assessed – this technique could potentially help overcome that.” The technique uses fluorescent markers that attach themselves to the relevant cells and indicate the stage of cell death. The retina is then observed using a customised laser ophthalmoscope. Until now, this kind of technique has only been used in cells in the lab, rather than in live animals. This research is therefore the first ever in vivo demonstration of retinal nerve cell death in Alzheimer’s Disease. The method, demonstrated in an animal model, could not only refine diagnosis of neurodegenerative disorders and help track disease progress; it could also aid the assessment and development of new treatments. Although this paper outlines the technique in animal models (rats and mice), Professor Cordeiro’s team are further along with work using the same technique to detect and assess glaucoma, and will be conducting their first patient trials later this year. Professor Cordeiro added, “The equipment used for this research was customised to suit animal models but is essentially the same as is used in hospitals and clinics worldwide. It is also inexpensive and non-invasive, which makes us fairly confident that we can progress quickly to its use in patients. The research was published in the journal Cell Death & Disease. Research published in the journal Alzheimer’s and Dementia shows that a combination of nutrients developed at MIT has shown the potential to improve memory in Alzheimer’s patients by stimulating growth of new brain connections. Richard Wurtman, the Cecil H. Green Distinguished Professor of Brain and Cognitive Sciences, did the basic research that led to the new experimental treatment. In a clinical trial of 225 Alzheimer’s patients, researchers found that a cocktail of three naturally occurring nutrients believed to promote growth of those connections, known as synapses, plus other ingredients (B vitamins, phospholipids and antioxidants), improved verbal memory in patients with mild Alzheimer’s. “If you can increase the number of synapses by enhancing their production, you might to some extent avoid that loss of cognitive ability,” says Wurtman. There is currently no cure for Alzheimer’s disease, though some medications can slow the progression of the disease. In particular, many U.S. patients take cholinesterase inhibitors, which increase levels of acetylcholine, a neurotransmitter important for learning and memory.
While those treatments target the symptoms of Alzheimer’s, Wurtman hopes to attack what he believes is the root cause of the disease: loss of synapses. The three nutrients in his dietary cocktail — uridine, choline and the omega-3 fatty acid DHA (all normally present in breast milk) — are precursors to the fatty molecules that make up brain cell membranes, which form synapses. In animal studies, Wurtman has shown that these nutrients boost the number of dendritic spines (small outcroppings of neural membranes). When those spines contact another neuron, a synapse is formed. Three additional clinical studies in Alzheimer’s patients are now underway, one in the United States and two in Europe. Results are expected to be available between 2011 and 2013. The first clinical study was sponsored by the French company Danone, known in the United States as Dannon; the study was conducted primarily in Europe and was led by Philip Scheltens, director of the Alzheimer Center at Vrije Universiteit Medical Center in Amsterdam. Wurtman and MIT have patented the mixture of nutrients used in the study, and Nutricia Advanced Medical Nutrition, a unit of Danone, holds the exclusive license on the patent. Patients with mild Alzheimer’s drank the cocktail (made in the form of a nutrient drink called Souvenaid, with the collaboration of Danone) or a control beverage daily for 12 weeks. Patients who received the nutrients showed a statistically significant level of improvement compared to control subjects: 40 percent of the treated patients improved performance in a test of verbal memory (memory for words, as opposed to memory of locations or experiences) known as the Wechsler Memory Scale, while 24 percent of patients who received the control drink improved their performance. Among those who received the cocktail, patients with the mildest cases of Alzheimer’s showed the most improvement. The drink appeared to have no effect on patients’ performance in another commonly used evaluation for Alzheimer’s patients, the ADAS-cog test. Wurtman believes that is because ADAS-cog is a more general assessment that tests for orientation and movement/spatial memory as well as cognition. So in subjects with early Alzheimer’s who show principally cognitive changes, more than the 225 subjects in the first study will probably be required to yield significant ADAS-cog changes after Souvenaid. The 500 subjects in the ongoing study in the United States may be sufficient. John Growdon, a neurologist at Massachusetts General Hospital, says that trying to regrow synapses is an innovative strategy and offers a complementary approach to two other lines of attack in treating Alzheimer’s: targeting the amyloid plaques that accumulate in patients’ brains, and minimizing the damage done by toxic metabolites that build up in Alzheimer’s-affected brains. “I don’t think any one approach has a monopoly, and that’s good,” Growdon says. “You need to have a lot of different approaches because no one knows what’s going to work.” Wurtman believes his approach to Alzheimer’s may eventually prove beneficial in treating other diseases. If these nutrients prove to be successful in Alzheimer’s patients, “then you can think about other diseases in which there are too few synapses,” such as Parkinson’s disease, he says. “There are a lot of diseases associated with synapse deficiency.” London writer Herman Goodden captures the fiendish nature of Alzheimer’s disease most eloquently in his article entitled “No place like home for victims of Alzheimer’s.” Writes Goodden, Alzheimer’s “doesn’t relent once it’s taken away 50 or 80 or 90% of your brain function and then lets you get on with what’s left. Sooner or later it will erase not just every memory and thought but also the workings of every last neuron and synapse.
here is no cure for Alzheimer’s, the insidious fatal disease which slowly kills all your brain cells. Already the seventh leading cause of death in the US, it is soon to reach epidemic levels as the boomers becomes senior citizens. There are more than 30 million people with dementia worldwide, but by 2050, this figure will increase to over 100 million. Two sets of findings released in the last few days bring hope that the accelerating research effort will find better ways to treat the disease, delay its onset, or prevent it from developing. Most significantly, a simple and inexpensive eye test could aid detection and diagnosis of Alzheimer’s at an earlier stage than is currently possible and a “cocktail” of commonly available supplements has shown promise in improving memory and fighting Alzheimer’s. Alzheimer’s disease was named after German physician Alois Alzheimer, who first described it in 1906. In the subsequent century, we’ve learned a lot about Alzheimer’s but with the ageing of the global population, it is about to become an epidemic. Currently there are more than 30 million people with dementia worldwide. By 2050, this figure will increase to over 100 million. Alzheimer’s is the most common form of dementia, accounting for 50 to 70 percent of dementia cases. It destroys brain cells, causing memory loss and problems with thinking and behavior severe enough to affect work, lifelong hobbies and social life. Alzheimer’s gets worse over time, and keeps destroying brain cells until there are none left. Accordingly, it is inevitably fatal with a mean life expectancy following diagnosis of approximately seven years. Today it is the seventh-leading cause of death in the United States. The most novel concept to come out of the three sets of research published in the last week is from University College London, where researchers have demonstrated a new technique that enables retinal, and therefore brain cell death, to be directly measured in real time. Few people realize that the retina is a direct, albeit thin, extension of the brain. It is entirely possible that in the future a visit to a high-street optician to check on your eyesight will also be a check on the state of your brain.“The death of nerve cells is the key event in all neurodegenerative disorders – but until now it has not been possible to study cell death in real time”, said Professor Cordeiro, of the UCL Institute of Ophthalmology.“This technique means we should be able to directly observe retinal nerve cell death in patients, which has a number of advantages in terms of effective diagnosis.
This could be critically important since identification of the early stages could lead to successful reversal of the disease progression with treatment. Currently, the biggest obstacle to research into new treatments for neurodegenerative diseases is the lack of a technique where the brain’s response to new treatments can be directly assessed – this technique could potentially help overcome that.” The technique uses fluorescent markers that attach themselves to the relevant cells and indicate the stage of cell death. The retina is then observed using a customised laser ophthalmoscope. Until now, this kind of technique has only been used in cells in the lab, rather than in live animals. This research is therefore the first ever in vivo demonstration of retinal nerve cell death in Alzheimer’s Disease. The method, demonstrated in an animal model, could not only refine diagnosis of neurodegenerative disorders and help track disease progress; it could also aid the assessment and development of new treatments. Although this paper outlines the technique in animal models (rats and mice), Professor Cordeiro’s team are further along with work using the same technique to detect and assess glaucoma, and will be conducting their first patient trials later this year. Professor Cordeiro added, “The equipment used for this research was customised to suit animal models but is essentially the same as is used in hospitals and clinics worldwide. It is also inexpensive and non-invasive, which makes us fairly confident that we can progress quickly to its use in patients. The research was published in the journal Cell Death & Disease. Research published in the journal Alzheimer’s and Dementia shows that a combination of nutrients developed at MIT has shown the potential to improve memory in Alzheimer’s patients by stimulating growth of new brain connections. Richard Wurtman, the Cecil H. Green Distinguished Professor of Brain and Cognitive Sciences, did the basic research that led to the new experimental treatment. In a clinical trial of 225 Alzheimer’s patients, researchers found that a cocktail of three naturally occurring nutrients believed to promote growth of those connections, known as synapses, plus other ingredients (B vitamins, phospholipids and antioxidants), improved verbal memory in patients with mild Alzheimer’s. “If you can increase the number of synapses by enhancing their production, you might to some extent avoid that loss of cognitive ability,” says Wurtman. There is currently no cure for Alzheimer’s disease, though some medications can slow the progression of the disease. In particular, many U.S. patients take cholinesterase inhibitors, which increase levels of acetylcholine, a neurotransmitter important for learning and memory.
While those treatments target the symptoms of Alzheimer’s, Wurtman hopes to attack what he believes is the root cause of the disease: loss of synapses. The three nutrients in his dietary cocktail — uridine, choline and the omega-3 fatty acid DHA (all normally present in breast milk) — are precursors to the fatty molecules that make up brain cell membranes, which form synapses. In animal studies, Wurtman has shown that these nutrients boost the number of dendritic spines (small outcroppings of neural membranes). When those spines contact another neuron, a synapse is formed. Three additional clinical studies in Alzheimer’s patients are now underway, one in the United States and two in Europe. Results are expected to be available between 2011 and 2013. The first clinical study was sponsored by the French company Danone, known in the United States as Dannon; the study was conducted primarily in Europe and was led by Philip Scheltens, director of the Alzheimer Center at Vrije Universiteit Medical Center in Amsterdam. Wurtman and MIT have patented the mixture of nutrients used in the study, and Nutricia Advanced Medical Nutrition, a unit of Danone, holds the exclusive license on the patent. Patients with mild Alzheimer’s drank the cocktail (made in the form of a nutrient drink called Souvenaid, with the collaboration of Danone) or a control beverage daily for 12 weeks. Patients who received the nutrients showed a statistically significant level of improvement compared to control subjects: 40 percent of the treated patients improved performance in a test of verbal memory (memory for words, as opposed to memory of locations or experiences) known as the Wechsler Memory Scale, while 24 percent of patients who received the control drink improved their performance. Among those who received the cocktail, patients with the mildest cases of Alzheimer’s showed the most improvement. The drink appeared to have no effect on patients’ performance in another commonly used evaluation for Alzheimer’s patients, the ADAS-cog test. Wurtman believes that is because ADAS-cog is a more general assessment that tests for orientation and movement/spatial memory as well as cognition. So in subjects with early Alzheimer’s who show principally cognitive changes, more than the 225 subjects in the first study will probably be required to yield significant ADAS-cog changes after Souvenaid. The 500 subjects in the ongoing study in the United States may be sufficient. John Growdon, a neurologist at Massachusetts General Hospital, says that trying to regrow synapses is an innovative strategy and offers a complementary approach to two other lines of attack in treating Alzheimer’s: targeting the amyloid plaques that accumulate in patients’ brains, and minimizing the damage done by toxic metabolites that build up in Alzheimer’s-affected brains. “I don’t think any one approach has a monopoly, and that’s good,” Growdon says. “You need to have a lot of different approaches because no one knows what’s going to work.” Wurtman believes his approach to Alzheimer’s may eventually prove beneficial in treating other diseases. If these nutrients prove to be successful in Alzheimer’s patients, “then you can think about other diseases in which there are too few synapses,” such as Parkinson’s disease, he says. “There are a lot of diseases associated with synapse deficiency.” London writer Herman Goodden captures the fiendish nature of Alzheimer’s disease most eloquently in his article entitled “No place like home for victims of Alzheimer’s.” Writes Goodden, Alzheimer’s “doesn’t relent once it’s taken away 50 or 80 or 90% of your brain function and then lets you get on with what’s left. Sooner or later it will erase not just every memory and thought but also the workings of every last neuron and synapse.
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