Scientists have spotted changes in brain activity that may point to Alzheimer’s.
Right now, the most widely accepted theory behind the cause of Alzheimer’s disease includes the build-up of amyloid-beta and tau proteins in the brain.
- Scientists
are still not clear as to how these two proteins might cause Alzheimer’s
disease.
- Researchers
from McGill University found people with increased levels of both
amyloid-beta and tau proteins in the brain may lead to changed brain
activity before the cognitive symptoms of Alzheimer’s disease appear.
Currently, the most widely accepted theory on what
causes Alzheimer’s disease revolves
around the
However, there are still questions on how amyloid
plaques and tau tangles might cause this type of dementia.
“The role of amyloid-beta and tau proteins in
Alzheimer’s disease has been well-established for decades,” Sylvain Baillet, PhD, professor of neurology
and neurosurgery, and computer science and associate dean of research in the
Faculty of Medicine & Health Sciences at McGill University in Canada
explained to Medical
News Today.
“While amyloid starts accumulating early in the aging
brain, it alone isn’t enough to cause Alzheimer’s. The accumulation of tau
comes later, and together, these proteins are present in the brains of
Alzheimer’s patients. However, how the earliest deposits of both proteins
affect brain activity in humans, especially before cognitive symptoms appear,
wasn’t well understood,” he said.
Baillet is the senior author of a new study recently
published in the journal
The study found that increased levels of both
amyloid-beta and tau proteins in the brain may lead to changed brain activity
before the cognitive symptoms of Alzheimer’s disease appear.
Focusing on
amyloid-beta and tau proteins
For this study,
researchers recruited 104 people who had a family history of Alzheimer’s
disease. All study participants received positron emission tomography (PET) to look
for any signs of the two proteins in the brain, as well as
“Amyloid-beta and tau proteins are naturally found in
the brain, but in Alzheimer’s disease, they both start to accumulate, possibly
because brain activity is altered early in the disease and/or these
accumulations modify brain activity, leading to a form of pathological chain
reaction,” Baillet explained.
AMYLOID-BETA VS. TAU PROTEINS
“Amyloid-beta
is a protein that can become sticky and form plaques between brain cells. These
plaques block communication between cells and can cause inflammation, which
damages the brain over time. Tau is a protein that usually helps support the
internal structure of brain cells. In Alzheimer’s, tau proteins start to tangle
inside the cells, disrupting their function and eventually leading to cell
death.”— Sylvain Baillet, PhD
Brain
slowing found in areas with both proteins
At the study’s
conclusion, Baillet and his team found that the brain areas within participants
with increased levels of amyloid-beta show signs of brain hyperactivity.
However, those with higher levels of both amyloid-beta
and tau proteins experienced hypoactivity or brain slowing. The researchers
used cognitive tests and found hypoactivity study participants also had
increased levels of attention and memory decline.
“We weren’t entirely surprised by this finding, but it
was significant to observe it so clearly in humans,” Baillet said. “Animal
models had predicted that amyloid-beta would accelerate brain activity, while
the combination of amyloid-beta and tau would eventually lead to hypoactivity,
or slowing of brain activity. However, this had not been directly observed in
human subjects until now.”
“What was surprising was
the extent to which this early slowing of brain activity in the presence of
both proteins was predictive of later cognitive decline — three to four years
after the MEG brain scans were collected. This connection between the early
buildup of amyloid-beta and tau, changes in brain activity, and later memory
and attention deficits highlights just how important it is to understand these
proteins’ impact on the brain, and how brain activity may alter in a subtle
fashion, long before symptoms appear.”— Sylvain Baillet, PhD
Baillet said their next research steps involve
continuing to follow the same participants over nearly 10 years, with follow-up
MEG scans, amyloid, and tau PET imaging, and detailed cognitive testing
currently being performed.
“Using these unique datasets from the
More
research still needed
MNT also spoke with Clifford Segil, DO,
neurologist at Providence Saint John’s Health Center in Santa Monica, CA, about
this study.
“This is a creative study which leaves me asking how
the authors determined that its participants would have long-term cognitive
declines as the data I reviewed noted its participants scored on average a 28.1
out of 30 on a
“When I reviewed this paper, I (was) left confused how
the authors determined that its participants would have ‘longitudinal declines’
or worsening memory loss as the belief that brain amyloid and tau levels always
cause cognitive issues remains controversial,” he continued.
“Many clinical neurologists like me remain unconvinced
that the build of any brain proteins is pathological and leads to cognitive
decline. As the clinical use of
Segil said he would like to see follow-up cognitive
testing done to determine if patients with high brain amyloid or tau have poor
cognition, as practicing neurologists continue to believe that brain amyloid is
not directly proportional to cognitive burden.
“The clinical use of
anti-brain amyloid medications [in] the United States is demonstrating that the
patients receiving these anti-amyloid medications are without any noticeable
changes in [cognition], supporting clinician’s positions that brain amyloid and
tau are less likely to be toxic or cause dementia’s cognitive symptoms.”—
Clifford Segil, DO
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