New Alzheimer’s Research Gives Hope for Early Intervention
U.S. researchers have shown that it may be possible to detect hints of Alzheimer’s disease nearly two decades before symptoms manifest, providing a vital window of opportunity for medical intervention.
Alzheimer’s disease most often affects the over 65s. It is a degenerative disorder, for which there is currently no cure, that leads to progressively worsening cognitive impairment. This often manifests in lapses in memory and thinking skills and a loss of physical dexterity to the point where, in the final stages before death, the sufferer becomes completely dependent on caregivers in order to have their basic needs met.
Treating the disease early is absolutely vital in order to slow down degeneration.
With this in mind, early detection of and intervention against Alzheimer’s has been a keen area of interest for researchers. Previous studies have shown that Alzheimer’s may be detectable up to 15 years prior to the disease manifesting when, as a result of brain cell death, the impairment becomes recognizable.
Now, U.S. researchers have been able to demonstrate that changes in brain chemistry in some Alzheimer’s sufferers may occur as much as two decades before clinical symptoms show themselves.
Researchers from Banner Alzheimer’s Institute in Arizona discovered this by taking a group of patients who have what is known as familial Alzheimer’s. There is a particular genetic mutation (PSEN1) which means that each person in that line will nearly always show signs of Alzheimer’s by their early 40s, this being what is known early on-set Alzheimer’s, a much rarer form of the disease.
The patients, a group of 20 people aged between 18 and 26 who all tested as having the mutation, were subjected to brain scans. Startlingly, when researchers compared the results of those brain scans with 24 people who did not have the genetic mutation, there were very clear differences in particular regions of the brain.
Specifically, carriers of the gene mutation were shown to have less brain matter in certain areas. They also displayed greater activity in the hippocampus and the parahipppcampus regions. In addition to this, the mutation carriers also exhibited a higher level of a protein called amyloid beta in their cerebrospinal fluid.
Amyloid beta has been detected in previous studies as an indicator of Alzheimer’s, but the test group showed an increase in the protein without the associated development of ”plaques” that are also key sign of Alzheimer’s.
While this research has only limited implications for Alzheimer’s detection in the wider population, researchers are hopeful it may provide the first steps to giving at-risk patients a window of opportunity to stave off cognitive degeneration.
Dr Eric Reiman, one of the scientists involved, said: “These findings suggest that brain changes begin many years before the clinical onset of Alzheimer’s disease.
“They raise new questions about the earliest brain changes involved in the predisposition to Alzheimer’s and the extent to which they could be targeted by future prevention therapies.”
Prof Nick Fox, from the Institute of Neurology at University College London, said some of his patients had lost a fifth of some parts of their brain by the time they arrived at the clinic.
He told the BBC: “I don’t think this pushes us forwards in terms of early diagnosis, we already have markers of the disease.
“The key thing this does is open up the window of early intervention before people take a clinical and cognitive hit.”
Finding a drug treatment for Alzheimer’s disease has proved notoriously difficult. This is partly because Alzheimer’s is usually only diagnosed after cognitive impairment has started, meaning the disease has already taken hold.
The presence of increased amyloid beta in the patients tested here, who may be as much as twenty to thirty years away from developing symptoms, has given researchers an avenue for future exploration because it suggests that Alzheimer’s may go through a longer pre-symptom period than first thought.
As such, timing may be crucial in blocking the accumulation of the protein that, researchers believe, triggers the disease mechanism. If researchers were able to intervene early enough, and with appropriate drug therapies, they may have a better chance of fighting Alzheimer’s progression.
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