Posts tagged memory impairment
Articles and news from the latest research reports.
Think You Have Alzheimer’s? UK Study Suggests You May Be Right
New research by scientists at the University of Kentucky’s Sanders-Brown Center on Aging suggests that people who notice their memory is slipping may be on to something.
The research, led by Richard Kryscio, Ph.D., chair of the Department of of Biostatistics and associate director of the Alzheimer’s Disease Center at UK, appears to confirm that self-reported memory complaints are strong predictors of clinical memory impairment later in life.
Kryscio and his group asked 531 people with an average age of 73 and free of dementia if they had noticed any changes in their memory in the prior year. The participants were also given annual memory and thinking tests for an average of 10 years. After death, participants’ brains were examined for evidence of Alzheimer’s disease.
During the study, 56 percent of the participants reported changes in their memory, at an average age of 82. The study found that participants who reported changes in their memory were nearly three times more likely to develop memory and thinking problems. About one in six participants developed dementia during the study, and 80 percent of those first reported memory changes.
"What’s notable about our study is the time it took for the transition from self-reported memory complaint to dementia or clinical impairment — about 12 years for dementia and nine years for clinical impairment — after the memory complaints began," Kryscio said. "That suggests that there may be a significant window of opportunity for intervention before a diagnosable problem shows up."
Kryscio points out that while these findings add to a growing body of evidence that self-reported memory complaints can be predictive of cognitive impairment later in life, there isn’t cause for immediate alarm if you can’t remember where you left your keys.
"Certainly, someone with memory issues should report it to their doctor so they can be followed. Unfortunately, however, we do not yet have preventative therapies for Alzheimer’s disease or other illnesses that cause memory problems."
The research, which was supported by grants from the National Institutes of Health, the National Institute on Aging, and the National Center for Advancing Translational Sciences, was published in the Sept. 24, 2014, online issue of Neurology.
(Source: uknow.uky.edu)
Alzheimer’s missing link found: Is a promising target for new drugs
Yale School of Medicine researchers have discovered a protein that is the missing link in the complicated chain of events that lead to Alzheimer’s disease, they report in the Sept. 4 issue of the journal Neuron. Researchers also found that blocking the protein with an existing drug can restore memory in mice with brain damage that mimics the disease.
“What is very exciting is that of all the links in this molecular chain, this is the protein that may be most easily targeted by drugs,” said Stephen Strittmatter, the Vincent Coates Professor of Neurology and senior author of the study. “This gives us strong hope that we can find a drug that will work to lessen the burden of Alzheimer’s.”
Scientists have already provided a partial molecular map of how Alzheimer’s disease destroys brain cells. In earlier work, Strittmatter’s lab showed that the amyloid-beta peptides, which are a hallmark of Alzheimer’s, couple with prion proteins on the surface of neurons. By an unknown process, the coupling activates a molecular messenger within the cell called Fyn.
In the Neuron paper, the Yale team reveals the missing link in the chain, a protein within the cell membrane called metabotropic glutamate receptor 5 or mGluR5. When the protein is blocked by a drug similar to one being developed for Fragile X syndrome, the deficits in memory, learning, and synapse density were restored in a mouse model of Alzheimer’s.
Strittmatter stressed that new drugs may have to be designed to precisely target the amyloid-prion disruption of mGluR5 in human cases of Alzheimer’s and said his lab is exploring new ways to achieve this.
Administering Natural Substance Spermidin Stopped Dementia
Scientists from Freie Universität Berlin and the University of Graz Have Shown That Feeding Fruit Flies with Spermidin Suppresses Age-dependent Memory Impairment
Age-induced memory impairment can be suppressed by administration of the natural substance spermidin. This was found in a recent study conducted by Prof. Dr. Stephan Sigrist from Freie Universität Berlin and the Neurocure Cluster of Excellence and Prof. Dr. Frank Madeo from Karl-Franzens-Universität Graz. Both biologists, they were able to show that the endogenous substance spermidine triggers a cellular cleansing process, which is followed by an improvement in the memory performance of older fruit flies. At the molecular level, memory processes in animal organisms such as fruit flies and mice are similar to those in humans. The work by Sigrist and Madeo has potential for developing substances for treating age-related memory impairment. The study was first published in the online version of Nature Neuroscience.
Aggregated proteins are potential candidates for causing age-related dementia. With increasing age, the proteins accumulate in the brains of fruit flies, mice, and humans. In 2009 Madeo’s group in Graz already found that the spermidin molecule has an anti-aging effect by setting off autophagy, a cleaning process at the cellular level. Protein aggregates and other cellular waste are delivered to lysosomes, the digestive apparatus in cells, and degraded.
Feeding the fruit flies spermidin significantly reduced the amount of protein aggregates in their brains, and their memories improved to juvenile levels. This can be measured because flies can learn under classical Pavovian conditioning and adjust their behavior accordingly.
In humans, memory capacity decreases beginnning around the age of 50. This loss accelerates with increasing age. Due to increasing life expectancy, age-related memory impairment is expected to increase drastically. The spermidine concentration increases with age in flies as in humans. If it were possible to delay the onset of age-related dementia by giving individuals spermidin as a food supplement, it would be a great breakthrough for individuals and for society. Patient studies are the next step for Sigrist and Madeo.
(Source: fu-berlin.de)
Common Food Supplement Fights Degenerative Brain Disorders
Nutritional supplement delays advancement of Parkinson’s and Familial Dysautonomia, TAU researchers discover
Widely available in pharmacies and health stores, phosphatidylserine is a natural food supplement produced from beef, oysters, and soy. Proven to improve cognition and slow memory loss, it’s a popular treatment for older people experiencing memory impairment. Now a team headed by Prof. Gil Ast and Dr. Ron Bochner of Tel Aviv University’s Department of Human Molecular Genetics has discovered that the same supplement improves the functioning of genes involved in degenerative brain disorders, including Parkinson’s disease and Familial Dysautonomia (FD).
In FD, a rare genetic disorder that impacts the nervous system and appears almost exclusively in the Ashkenazi Jewish population, a genetic mutation prevents the brain from manufacturing healthy IKAP proteins — which likely have a hand in cell migration and aiding connections between nerves — leading to the early degeneration of neurons. When the supplement was applied to cells taken from FD patients, the gene function improved and an elevation in the level of IKAP protein was observed, reports Prof. Ast. These results were replicated in a second experiment which involved administering the supplement orally to mouse populations with FD.
The findings, which have been published in the journal Human Molecular Genetics, are very encouraging, says Prof. Ast. “That we see such an effect on the brain — the most important organ in relation to this disease — shows that the supplement can pass through the blood-brain barrier even when administered orally, and accumulate in sufficient amounts in the brain.”
Slowing the death of nerve cells
Already approved for use as a supplement by the FDA, phosphatidylserine contains a molecule essential for transmitting signals between nerve cells in the brain. Prof. Ast and his fellow researchers decided to test whether the same chemical, which is naturally synthesized in the body and known to boost memory capability, could impact the genetic mutation which leads to FD.
Researchers applied a supplement derived from oysters, provided by the Israeli company Enzymotec, to cells collected from FD patients. Noticing a robust effect on the gene, including a jump in the production of healthy IKAP proteins, they then tested the same supplement on mouse models of FD, engineered with the same genetic mutation that causes the disease in humans.
The mice received the supplement orally, every two days for a period of three months. Researchers then conducted extensive genetic testing to assess the results of the treatment. “We found a significant increase of the protein in all the tissues of the body,” reports Prof. Ast, including an eight-fold increase in the liver and 1.5-fold increase in the brain. “While the food supplement does not manufacture new nerve cells, it probably delays the death of existing ones,” he adds.
Therapeutic potential for Parkinson’s
That the supplement is able to improve conditions in the brain, even when given orally, is a significant finding, notes Prof. Ast. Most medications enter the body through the blood stream, but are incapable of breaking through the barrier between the blood and the brain.
In addition, the researchers say the supplement’s positive effects extend beyond the production of IKAP. Not only did phosphatidylserine impact the gene associated with FD, but it also altered the level of a total of 2400 other genes — hundreds of which have been connected to Parkinson’s disease in previous studies.
The researchers believe that the supplement may have a beneficial impact on a number of degenerative diseases of the brain, concludes Prof. Ast, including a major potential for the development of new medications which would help tens of millions of people worldwide suffering from these devastating diseases.
(Source: aftau.org)