Neurodegenerative diseases such as Alzheimer’s and Parkinson’s can start assaulting brain cells many years before any outward signs of the damage are displayed.
That makes it difficult for doctors trying to come up with early diagnosis and possible interventions for millions of Americans.
Until recently, assorted memory and mental-processing tests were about the only tools doctors had to determine the onset of dementia, and it’s often hard to distinguish whether the problem is caused by the tangles and plaque buildup of Alzheimer’s, a stroke or some other medical condition, or even an adverse drug reaction.
Scientists have worked with some general measurements of brain-volume loss as a marker for disease, but without much precision. Over the last several years, though, researchers have begun to make strides using various brain-imaging tools to look at structures inside the skull.
Working through data compiled by numerous participants in the Alzheimer’s Disease Neuroimaging Initiative, scientists have made enough comparisons between images from scans and autopsies to start to understand what changes in the size or even energy consumption of different parts of the brain might mean.
One team at the University of California, San Diego, recently reported a fairly quick way to identify Alzheimer’s progression using magnetic resonance imaging.
The researchers found that changes in the brain’s memory regions, particularly a part of the temporal lobe called the entorhinal cortex, offer sensitive measures of early stages of the disease.
“The technique is extremely powerful, because it allows a researcher to examine exactly how much brain-volume loss has occurred in each region of the brain, including the cortical regions, where we know the bad proteins of Alzheimer’s disease build up,” said Dr. James Brewer, a neurologist and co-author of a study reporting the findings last month in the Proceedings of the National Academy of Science.
The scientists say the imaging markers not only track brain atrophy, “but distinguish the early states of Alzheimer’s disease from changes related to normal aging,’’ said Anders Dale, the professor of neuroscience and radiology who led the project.
Another group, at Washington University in St. Louis, moved detection ahead still further in mid-December with studies that show people with measurable levels of a protein associated with Alzheimer’s are at greater risk of developing the disease and for losing brain volume later on.
One project, done from 2004-08, tracked 159 volunteers ages 51-88 with no sign of cognitive impairment using scans that can detect the protein beta-amyloid in the brain, as well as MRIs to measure brain volume and standard memory and thinking tests.
Over time, 23 of the subjects developed mild cognitive impairment and nine were diagnosed with Alzheimer’s. All had relatively high levels of the protein compared with subjects who remained cognitively normal, but so, too, did some who didn’t become impaired.
Another study, of 135 volunteers ages 65-88, found that levels of the protein matched atrophy of brain regions associated with memory, and declining scores in thinking and memory tests over many years. The findings were published in the Archives of Neurology.
“These studies confirm the value of detecting and measuring amyloid load in the brains of living people as soon as possible,’’ said Dr. John Morris, who led one of the studies and heads the university’s Alzheimer’s Disease Research Center.
Meanwhile, neurologists at Penn State’s Hershey College of Medicine compared videos of walking movements of a small group of volunteers to those of a group diagnosed with Parkinson’s disease and found that the extent to which one arm swings versus the other while walking could represent a very early sign of the disease. The asymmetry in arm movement was much more noticeable in the subjects with Parkinson’s.
“Our data suggests this could be a very useful tool for early detection,’’ said Xuemei Huang, lead author of the report published in the journal Gait and Posture.
Such early diagnosis could be useful if widespread efforts to find drugs that can halt the death of dopamine-producing brain cells early in the course of Parkinson’s start to pay off, she said