Scientists have long fallen on their brains for ways to treat Alzheimer’s disease, the most common type of dementia.
It turns out that the answer can stay inside our brain. Researchers from the Northwestern University suggest that improvement of brain immune cells can better equip them to clear harmful clusters of beta amyloid toxic protein, a distinctive sign of Alzheimer’s.
“Our study is very young because we had the rare opportunity to analyze one of the largest groups of brain after the death of Alzheimer’s patients treated with target amiloid medicines similar to those now approved by FDA for Alzheimer’s disease,” said lead author Lynn van Olst.
Researchers examined 13 vaccinated brains with amyloid beta, six Alzheimer’s brain that did not receive that treatment and six brains without disease.
Amiloid beta is a small protein fragment that forms plaque -like deposits when accumulated abnormally in the brain. Vaccination is supposed to cause the immune system to produce antibodies to remove the plaques.
But clinical tests of beta amyloid vaccines for Alzheimer’s have failed continuously. Dangerous brain extension has been a major side effect.
The challenge for vaccine developers is to create an immune response that can fight amyloid beta without attacking healthy cells.
The US Food and Drug Administration has approved some antibody treatments for Alzheimer’s aimed at beta amyloid. They are given as intravenous infusions.
“These medicines stimulate brain immune cells to remove amyloid beta, but we believe that data in our publication can be used to make these medicines work even better,” said the relevant author of study David Gate, a Northwestern Assistant Professor of Neurology.
The northwestern team found that when these types of treatments work, brain immune cells – known as microglia – clear tiles and help restore a healthier brain environment.
Of the 13 vaccinated brains, seven had high levels of tile cleaning. The other six had limited cleaning.
“Our study is the first to identify mechanisms in microglia, brain immune cells, which help limit the spread of amyloid in certain regions of brain after treatment with target amiloid medication,” said Gate, the director of the abrams research center in neurogenomics.
The gate team found that only a few microglia is effective in removing tiles. Factors for success include brain region, type of immunization and gene activity.
The good news is that microglia is not always focused on removing amyloids.
“They can remove the amyloid and then come back to be good and seem to actually help the brain to heal,” Gate said.
The bad news is that the direct target of microglia is still a challenge.
“If we can determine the mechanisms that are associated with purification of the pathology, and we can find the genetic composition of immune cells that are associated with people who really respond well to the medicine, then perhaps one day we can bypass the whole process of medication and simply target these specific cells,” Gate said.
Gate’s conclusions were published on Thursday in natural medicine.
He told the post that the team is taking tissue of patients’ brain tissue receiving new anti-amiloid antibodies to explore their efficiency and are investigating how to apply these findings to other neurodegenerative diseases, such as Parkinson’s and ALS disease.
Alzheimer’s affects about 7 million Americans while nearly 1 million Americans are affected by Parkinson. Less than 30,000 Americans are believed to have ALS.
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