Biomarkers in cerebrospinal fluid may help predict a patient's progression from mild cognitive impairment (MCI) to Alzheimer's disease, according to a new study.
Previous research shows damage to axons and neurons in Alzheimer's disease begins decades before signs of the neurological condition appear.
Researchers from Sweden found the relative progression from MCI to Alzheimer's disease is significantly increased in patients with abnormal concentrations of certain biomarkers in their cerebrospinal fluid, which is the fluid between one's brain and spinal cord.
They say, "If validated in other consecutive studies with long follow-up, these results may have an effect both on the diagnostic work-up and on thee design of clinical trails of patients with mild cognitive impairment."
Nearly half of people between ages 90 and 95 are affected by dementia, and this study revealed nearly half of people with MCI develop Alzheimer's.
CHICAGO - The largest study to date of twins and Alzheimer's disease indicates that inheritance may play a role in nearly 80 percent of cases.
The report from the University of Southern California was based on a look at 392 pairs of twins in Sweden, age 65 and beyond, both identical and fraternal, at least one of whom had been diagnosed with Alzheimer's. They were compared to a similar group of twins who were free of the disease.
While genetics has already been linked to the disease the new research "confirms the higher estimates that have been suggested previously. The important thing is that no one has had this large a sample before," said lead author Margaret Gatz. She said the sample was 10 times larger than any other group of twins studied for the disease.
Gatz said the study "does suggest that there is an underlying genetic basis" but she cautioned "this doesn't mean that environment is not important. Environment may be relevant not only for whether but also for when one gets the disease."
The study, published in the Archives of General Psychiatry, concluded that heritability was "79 percent in the best fitting (analytical) model with the balance of variation explained by non-shared environmental influences."
In a second study published in the same journal, researchers at Mount Sinai School of Medicine, New York, found that people who suffer from depression throughout their life and later develop Alzheimer's show more physical changes in their brain than those with the disease who did not have depression.
Those with depression also suffer a more rapid mental decline once they develop the disease, said the study which was based on more than 90 Alzheimer patients, some of whom had lifetime depression and others who did not.
Previous studies have linked depression and Alzheimer's disease, the study added.
March 13 2003 - Common pain pills such as ibuprofen and naproxen may actually dissolve the brain lesions that clog the brains of Alzheimer's patient, U.S. researchers have reported.
The findings may help explain studies that suggest people who frequently take the aspirin-like pills seem to have a lower risk of Alzheimer's, which affects an estimated 4 million Americans.
Writing in the journal Neuroscience, the team at the University of California Los Angeles said they made the discovery using a new chemical marker called FDDNP.
It attaches to the amyloid plaques that mark Alzheimer's, allowing scientists to watch their progression. These plaques eventually kill brain cells, leading to the progressive loss of memory and brain function that debilitates and kills Alzheimer's patients.
Using brain tissue in laboratory dishes, the team showed that FDDNP goes straight for the damaging protein plaques. When they added ibuprofen and other non-steroidal anti-inflammatory drugs, the plaques seemed to break up.
There is currently no cure for Alzheimer's and treatments only improve symptoms for a short time.
"This would provide hope to patients and families by modifying outcomes," Barrio said in a statement.
"This new technology will likely help us monitor new vaccines and drugs designed to prevent and treat the brain damage caused by Alzheimer's disease," added Dr. Gary Small, a professor of psychiatry who worked on the study.
Feb. 2 2006 - When an Arctic ground squirrel hibernates, its body temperature drops below the freezing point of water and the blood-flow through its brain slows to a trickle. Though the squirrel's brain survives, it loses many of the nerve-cell connections that govern how it operates. The brain regenerates itself soon after the animal emerges from its long sleep. Exactly how is a matter of intense research but one group of scientists thinks that part of the explanation lies with a protein associated with Alzheimer's disease. And that raises the hope that the ravages wrought on the human mind by Alzheimer's disease could be as reversible as the winter freeze.
Arctic ground squirrels hibernate for up to seven months of the year, sinking into a torpor from which they periodically rewarm their bodies to 37°C before re-entering the supercooled state. Research has shown that during hibernation these animals lose memories they laid down beforehand and also their ability to form new ones. This loss must be temporary, however, or the animal would become more amnesic with each hibernation.
The brain stores information in neuronal networks. The chemical connections between neurons, called synapses, are thought to be critical to the formation of those networks and hence the laying down of memories. In 2003 a group led by Thomas Arendt of the University of Leipzig in Germany showed that the number of synapses in the hippocampus, a brain structure crucial for learning and memory, falls during hibernation. This is partly because hippocampal neurons lose many of their branching projections, or dendrites, and so provide less opportunity for forming synapses with neighbouring neurons.
All that changes within two or three hours of an animal emerging from hibernation, when a wave of new growth ensures that the number of synapses in the hippocampus soars beyond even pre-hibernation levels. The next 20 hours see a pruning back of those connections, rather as in the very young human brain. Just as in that developmental process, the new synapses seem to enhance memory only once the pruning has taken place.
Nobody knows what triggers these dramatic morphological changes in the hippocampus during and after hibernation. But Dr Arendt's group has made the startling discovery that hibernating brains accumulate a protein called hyperphosphorylated tau. This protein is known also to accumulate in the neurons that degenerate in the brains of people with Alzheimer's disease. Notably, though by no means exclusively, it accumulates in the hippocampal neurons, where it is associated with the formation of lesions.
There are several competing theories about what causes Alzheimer's disease. One possibility is that the tau protein causes the lesions in the brain. Another is that something else causes the lesions, and the tau protein is the brain's defence against that attack. Thus, it is possible that the tau protein might not be the problem, but rather a symptom of the problem.
During hibernation, the levels of tau protein in a squirrel's hippocampal cells are directly correlated with the loss of synapses but not with the appearance of lesions. On emerging from hibernation, the squirrel eliminates the tau protein from its brain. This has led Dr Arendt to suggest that rather than being a part of a disease process, the formation of the tau protein could be a mechanism by which the brain protects itself. He argues that the brain is armed with mechanisms for clearing the tau protein and that the reason it doesn't in people with Alzheimer's disease is because the protein is protecting the neurons.
His stance is contentious. "As the field stands, viewing pathology as anything other than pathogenic is controversial. Saying it is protective is heretical," says Mark Smith of Case Western Reserve University in Cleveland, Ohio. He has conducted studies on living neurons which suggest that the tau protein is produced in response to oxidative stress, thus lending support to the protective hypothesis.
Dr Arendt's group is now engaged in discovering exactly how the tau protein can be cleared from the brain. Help for Alzheimer's patients remains uncertain and a very long way off, but spring seems to have come a bit closer.
