“Alzheimer's disease has
long been characterized by the buildup of two distinct proteins in the brain:
first beta-amyloid, which accumulates in clumps, or plaques, and then tau,
which forms toxic tangles that lead to cell death. But how beta-amyloid leads to
the devastation of tau has never been precisely clear. Now a new study at the
University of Alabama at Birmingham appears to describe that missing mechanism.
“The study details a cascade of
events. Buildup of beta-amyloid activates a receptor that responds to a brain
chemical called norepinephrine, which is commonly known for mobilizing the
brain and body for action. Activation of this receptor by both beta-amyloid and
norepinephrine boosts the activity of an enzyme that activates tau and
increases the vulnerability of brain cells to it, according to the study,
published in Science Translational
Medicine.
“Essentially, beta-amyloid hijacks the
norepinephrine pathway to trigger a toxic buildup of tau, says Qin Wang, the
study’s senior author and a professor of neuropharmacology in the department of
cell, developmental and integrative biology at the University of Alabama at
Birmingham. ‘We really show
that this norepinephrine is a missing piece of this whole Alzheimer’s disease
puzzle,’ she says…”
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