Could the Immune System Be Key to Alzheimer’s Disease?
Article posted yesterday in Discover Magazine. I know that Alzheimer's is an indication that has been previously discussed, but there is some high tech info in this article that relates to recent posts here. The author discusses CD 4, CD 8, T cells, etc. I wonder how the market potential for Alzheimer's compares to HIV and cancer?
Link and excerpts follow.
https://www.discovermagazine.com/mind/could-t...rs-disease
For nearly 30 years, the hunt for a cure for Alzheimer’s disease has focused on a protein called beta-amyloid. Amyloid, the hypothesis goes, builds up inside the brain to bring about this memory-robbing disorder, which afflicts some 47 million people worldwide.
Billions of dollars have poured into developing therapies aimed at reducing amyloid — thus far, to no avail. Trials of anti-amyloid treatments have repeatedly failed to help patients, sparking a reckoning among the field’s leaders.
With the field’s thinking narrowed around the amyloid hypothesis, immunological ideas have struggled to win favor — and funding. “There was no traction,” says Malú Tansey, a University of Florida neuroscientist whose work focuses on immunology of the brain. The committees that review grant applications didn’t want to hear about immunological studies, she says.
But over the past decade, the immune system connection to Alzheimer’s has become clearer. In several massive studies that analyzed the genomes of tens of thousands of people, many DNA variants that were linked to heightened Alzheimer’s risk turned out to be in genes involved in immunity — specifically, a branch of the body’s defenses known as the innate immune system. This branch attacks viruses, bacteria and other invaders quickly and indiscriminately. It works, in part, by triggering inflammation.
A further connection between inflammation and Alzheimer’s turned up in March 2020, in an analysis of electronic health records from 56 million patients, including about 1.6 million with rheumatoid arthritis, psoriasis and other inflammatory diseases. When researchers searched those records for Alzheimer’s diagnoses, they found that patients taking drugs that block a key molecular trigger of inflammation, called tumor necrosis factor (TNF), have about 50 to 70 percent lower odds of having an Alzheimer’s diagnosis than patients who were prescribed those drugs but did not take them.
This newer wave of studies opened people’s eyes to the idea that the immune system might be a major driver of Alzheimer’s pathology, says Sharon Cohen, a behavioral neurologist who serves as medical director at the Toronto Memory Program in Canada. Over time, Cohen says, researchers began thinking that “maybe inflammation is not just an aftereffect, but actually a pivotal, early effect.”
Article posted yesterday in Discover Magazine. I know that Alzheimer's is an indication that has been previously discussed, but there is some high tech info in this article that relates to recent posts here. The author discusses CD 4, CD 8, T cells, etc. I wonder how the market potential for Alzheimer's compares to HIV and cancer?
Link and excerpts follow.
https://www.discovermagazine.com/mind/could-t...rs-disease
For nearly 30 years, the hunt for a cure for Alzheimer’s disease has focused on a protein called beta-amyloid. Amyloid, the hypothesis goes, builds up inside the brain to bring about this memory-robbing disorder, which afflicts some 47 million people worldwide.
Billions of dollars have poured into developing therapies aimed at reducing amyloid — thus far, to no avail. Trials of anti-amyloid treatments have repeatedly failed to help patients, sparking a reckoning among the field’s leaders.
With the field’s thinking narrowed around the amyloid hypothesis, immunological ideas have struggled to win favor — and funding. “There was no traction,” says Malú Tansey, a University of Florida neuroscientist whose work focuses on immunology of the brain. The committees that review grant applications didn’t want to hear about immunological studies, she says.
But over the past decade, the immune system connection to Alzheimer’s has become clearer. In several massive studies that analyzed the genomes of tens of thousands of people, many DNA variants that were linked to heightened Alzheimer’s risk turned out to be in genes involved in immunity — specifically, a branch of the body’s defenses known as the innate immune system. This branch attacks viruses, bacteria and other invaders quickly and indiscriminately. It works, in part, by triggering inflammation.
A further connection between inflammation and Alzheimer’s turned up in March 2020, in an analysis of electronic health records from 56 million patients, including about 1.6 million with rheumatoid arthritis, psoriasis and other inflammatory diseases. When researchers searched those records for Alzheimer’s diagnoses, they found that patients taking drugs that block a key molecular trigger of inflammation, called tumor necrosis factor (TNF), have about 50 to 70 percent lower odds of having an Alzheimer’s diagnosis than patients who were prescribed those drugs but did not take them.
This newer wave of studies opened people’s eyes to the idea that the immune system might be a major driver of Alzheimer’s pathology, says Sharon Cohen, a behavioral neurologist who serves as medical director at the Toronto Memory Program in Canada. Over time, Cohen says, researchers began thinking that “maybe inflammation is not just an aftereffect, but actually a pivotal, early effect.”
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