An estimated 5.3 million in the U.S. have Alzheimer’s disease now, according to the Alzheimer’s Association. By 2050, that number may rise to 11 or 16 million, barring advances to treat the irreversible brain disorder marked by decline in memory and other cognitive skills.
Identifying those at risk for Alzheimer’s, as well as finding new treatments, is a ”social imperative,” said Sam Sisodia, Ph.D., a researcher at the University of Chicago and moderator of a news conference Monday at the annual meeting of the Society for Neuroscience in San Diego.
Among the research updates, all presented at the meeting:
- Findings about structural changes in Alzheimer’s patients in a brain area typically associated with Parkinson’s disease and other movement disorders;
- New discoveries that there is structural change in parts of the cerebral cortex charged with reasoning, memory and other ”higher function” tasks in people at risk for the disease;
- Findings that small clumps of a protein in the brain (already linked with Alzheimer’s) interfere with memory, and so may be a good target for new drugs;
- A new vaccine in early studies that may work without dangerous side effects.
Patients with Alzheimer’s disease, compared to those who are healthy or who had mild cognitive impairment, which sometimes precedes Alzheimer’s, had a smaller caudate nucleus, said Sarah Madsen, a graduate student at the University of California Los Angeles.
She compared 100 healthy elderly people, 200 with impairment and 100 with diagnosed Alzheimer’s, performing brain scans. Her findings echoed previous studies.
”We found the caudate nucleus is 7 percent smaller in those with Alzheimer’s compared to controls,” she said. That could mean Alzheimer’s produces broader damage in the brain that experts thought, she said.
Brain changes also show up in those at risk for the disease, said Sarah George, a graduate student at Rush University Medical Center, Chicago, who reported on her study of 52 people with a condition called amnestic mild cognitive impairment and thought at high risk.
Some with this condition progress to Alzheimer’s, but not all. These patients were followed for nearly 6 years; 23 progressed and 29 did not.
She looked for changes in structure in the brain area called the substantia innominata, an area deep in the brain. It sends chemical signals to the cerebral cortex, the outer layer of the brain, related to reasoning and memory.
Those who went on to develop Alzheimer’s had different images. “Although there were not structural changes in the substantia innominata, the cortical regions that receive strong input from this area are strongly vulnerable,” she said.
There was thinning of the cortical areas that receive input from the SI, she said.
Brains that have too many small aggregates of a a protein called tau, long linked with Alzheimer’s, may have memory problems, said Ottavio Arancio, M.D., Ph.D., a researcher at Columbia University in New York.
In his animal study, he found even small clumps of the tau protein may disrupt memory.
Tau and beta-amyloid are both proteins associated with the disease. Recently, experts have zeroed in on some smaller forms of these protein, and Arancio has targeted smaller forms which are outside cells.
These smaller forms could be especially toxic to neurons, he said.
In the past, vaccines for Alzheimer’s have not worked, and have caused dangerous autoimmune reactions and brain inflammation. But the vaccines typically target the human version of the beta-amyloid protein associated with the disease.
Charles Glabe, Ph.D., a researcher at the University of California, Irvine, reported success in an animal study of a vaccine developed against a non-human protein that is similar to beta-amyloid but has a different amino acid sequence.
He has tested it so far in mice, and found the animals have better memory and other cognitive skills and fewer clumps of beta-amyloid and tau protein.
Source: Society for Neuroscience