R & D
11/01/2017
by Kenny Walter - Digital Reporter - @RandDMagazine
https://www.rdmag.com/article/2017/11/alzheimers-may-not-originate-brain?et_cid=6158454&et_rid=280879682&type=cta&et_cid=6158454&et_rid=280879682&linkid=content
The long assumption that Alzheimer’s disease originates in the brain may not be true after all— as new findings indicate the disease could be triggered by breakdowns elsewhere in the body.
Researchers from the University of British Columbia (UBC) believe that the new discovery could lead to new drug therapies that may be able to stop or slow the disease down without acting directly on the brain, an often complex, sensitive and hard-to-reach target.
The researchers were able to demonstrate the cancer-like mobility of the disease with a technique called parabiosis—where they surgically attached two specimens together so they share the same blood supply for several months.
The researchers modified normal mice, which do not naturally develop Alzheimer’s, to carry a mutant human gene that produces high levels of a protein called amyloid-beta that ultimately forms clumps or plaques that smother brain cells in humans.
Amyloid-beta is produced in blood platelets, blood vessels and muscles and its precursor protein is found in several other organs.
However, until the current experiment it was unclear if the protein from outside the brain could contribute to Alzheimer’s disease.
“The blood-brain barrier weakens as we age,” UBC Psychiatry Professor Dr. Weihong Song, Ph.D., said in a statement. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”
The mice that had been joined to the genetically modified partners for a year ended of contracting Alzheimer’s disease. The amyloid-beta traveled from the genetically-modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.
Along with developing plaques, the mice also developed a pathology similar to tangles—twisted protein strands that form inside brain cells, disrupting their function and eventually killing them from the inside-out.
The mice also developed Alzheimer’s-like damage including brain cell degeneration, inflammation and microbleeds, as well as the impairment of the ability to transmit electrical signals involved in learning and memory—even in mice that had been joined for just four months.
According to Song, a potential drug could bind to amyloid-beta throughout the body, tagging it biochemically in a way that the liver or kidneys could clear it.
“Alzheimer's disease is clearly a disease of the brain but we need to pay attention to the whole body to understand where it comes from and how to stop it,” he said.
The study was published in Molecular Psychiatry
11/01/2017
by Kenny Walter - Digital Reporter - @RandDMagazine
https://www.rdmag.com/article/2017/11/alzheimers-may-not-originate-brain?et_cid=6158454&et_rid=280879682&type=cta&et_cid=6158454&et_rid=280879682&linkid=content
The long assumption that Alzheimer’s disease originates in the brain may not be true after all— as new findings indicate the disease could be triggered by breakdowns elsewhere in the body.
Researchers from the University of British Columbia (UBC) believe that the new discovery could lead to new drug therapies that may be able to stop or slow the disease down without acting directly on the brain, an often complex, sensitive and hard-to-reach target.
The researchers were able to demonstrate the cancer-like mobility of the disease with a technique called parabiosis—where they surgically attached two specimens together so they share the same blood supply for several months.
The researchers modified normal mice, which do not naturally develop Alzheimer’s, to carry a mutant human gene that produces high levels of a protein called amyloid-beta that ultimately forms clumps or plaques that smother brain cells in humans.
Amyloid-beta is produced in blood platelets, blood vessels and muscles and its precursor protein is found in several other organs.
However, until the current experiment it was unclear if the protein from outside the brain could contribute to Alzheimer’s disease.
“The blood-brain barrier weakens as we age,” UBC Psychiatry Professor Dr. Weihong Song, Ph.D., said in a statement. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”
The mice that had been joined to the genetically modified partners for a year ended of contracting Alzheimer’s disease. The amyloid-beta traveled from the genetically-modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.
Along with developing plaques, the mice also developed a pathology similar to tangles—twisted protein strands that form inside brain cells, disrupting their function and eventually killing them from the inside-out.
The mice also developed Alzheimer’s-like damage including brain cell degeneration, inflammation and microbleeds, as well as the impairment of the ability to transmit electrical signals involved in learning and memory—even in mice that had been joined for just four months.
According to Song, a potential drug could bind to amyloid-beta throughout the body, tagging it biochemically in a way that the liver or kidneys could clear it.
“Alzheimer's disease is clearly a disease of the brain but we need to pay attention to the whole body to understand where it comes from and how to stop it,” he said.
The study was published in Molecular Psychiatry