- Formation of amyloid plaques in the brain is now the leading theory for the cause of Alzheimer’s disease..
- Researchers at the USC Leonard Davis School have found that as the brain naturally ages, even healthy brains have higher levels of amyloid protein, which isn’t always a sign of Alzheimer’s disease.
- Instead, the problem may be the fact that some brains are unable to adequately clear the accumulated amyloid protein.
- The research team says their findings support the use of PET imaging to check the brain for elevated amyloid proteins and the development of drugs that directly target the cellular mechanisms that clear beta-amyloid.
We still don’t know exactly what causes a form of dementia called Alzheimer’s disease, but the prevailing theory continues to be that
Researchers at the USC Leonard Davis School are now working on higher-level
Researchers have shown that the soluble form of beta-amyloid is not correlated with Alzheimer’s disease mechanisms in the brain. associated with disease progression.
This is why the authors of the study believe the problem may lie in the reduced ability of some brains to clear this protein as it builds up.
This research recently
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Recent studies indicate that soluble beta-amyloid may play beneficial roles in neuronal and synaptic function. However, excess soluble beta-amyloid can be toxic to the brain.
Due to its molecular structure, beta-amyloid is known to be “sticky”. That means it can aggregate with other proteins to form amyloid plaques that deposit on the outside of neurons.
These amyloid plaques can impair neuronal function, but are less damaging to neuronal function than the soluble form. Some researchers believe that its formation is a protective mechanism that prevents the effects of excess soluble beta-amyloid.
For this study, researchers looked at postmortem brain tissue samples from people with healthy brains and from people with dementia who were between the ages of 66 and 99 at the time of death.
Upon analysis, scientists found a similar amount of soluble material.
“We were surprised by the extensive overlap in soluble or non-aggregated forms of amyloid protein between patients with normal cognition and those with Alzheimer’s disease,” said a postdoctoral researcher at the USC Leonard Davis School and Dr. Max Thorwald, lead author of the study, said. medical news today.
“We also found that the precursors of this protein were reduced in the brains of Alzheimer’s patients compared to normal cognitive function. [brains],” he added.
Additionally, researchers found high levels of beta-amyloid in the brain tissue of Alzheimer’s patients. So if elevated amyloid levels don’t explain the disease, what could it be?
“As expected, aggregated forms of these peptides increased in Alzheimer’s disease brains,” Dr. Thorwald said. “We hypothesize that decreased clearance of amyloid proteins also contributes to Alzheimer’s disease.”
“These findings further support the use of aggregated or fibrillar amyloid as biomarkers for the treatment of Alzheimer’s disease,” he added. “At sites where amyloid processing occurs, there are fewer precursors and enzymes available for processing, which may suggest amyloid clearance as a key problem in Alzheimer’s disease.”
The research team supports the use of positron emission tomography (PET) imaging in other individuals to confirm the presence of increased amyloid protein, regardless of whether their findings indicate symptoms of Alzheimer’s disease. I believe that
“[And] These findings suggest that new drugs may be developed for amyloid protein clearance to treat Alzheimer’s disease,” said Thorwald.
MNT We also spoke with Dr. Heather Snyder, vice president of medical and scientific relations at the Alzheimer’s Association, about the research.
She commented that these findings add to:
“This study further strengthens the idea that targeting clearing mechanisms in the brain may affect not only beta-amyloid, but the mechanisms themselves,” said Dr. Snyder. “There is ongoing early research that builds on the idea of stimulating and modifying clearance mechanisms as a potential strategy for treating Alzheimer’s disease.”
“The Alzheimer’s Association’s Part the Cloud program is funding research by Lyndon Lien, Ph.D., of Qinotto, Inc. He is conducting phase 1 research into an activating drug.
MNT We also spoke to Dr. David A. Merrill, a psychiatrist and director of the Pacific Brain Health Center at the Pacific Neuroscience Institute at Providence St. John’s Health Center in Santa Monica, California, about the study.
“It is interesting to read that soluble amyloid increases with normal aging, which suggests that amyloid may have some role in normal brain function with aging. , contrary to the idea that amyloid is the enemy and that the mere presence of amyloid matters: that you have Alzheimer’s disease.”
– Dr. David A. Merrill
Dr. Merrill said the research suggests that Alzheimer’s disease is the result of problems removing amyloid, resulting in plaque buildup.
“The implication is that treatments aimed at helping clear amyloid may help prevent the progression of Alzheimer’s disease,” he continued. This is consistent with new drugs that have been shown to help reduce the burden of amyloid plaques in the brain.”
“What the field needs is safe treatment. [and] It doesn’t cause massive brain swelling or cerebral hemorrhage,” Dr. Merrill added.
“And ideally, we would also see treatments that not only reduce the amount of amyloid deposits, slow their progression, but also improve the structure and function of the brain, such as improving neuronal function, improving memory. [However,] Slowing the progression is better than no treatment,” Merrill said.
