Reddy's paper
suggests that when the interaction between the phosphorylated tau and the
amyloid-beta -- particularly in its toxic form -- happens at brain synapses, it
can damage those synapses. And that can lead to cognitive decline in
Alzheimer's patients.
"This complex
formation between amyloid-beta and tau -- it is actually blocking the neural
communication," Reddy said. "If we could somehow find a molecule that
could inhibit the binding of these two proteins at the synapses, that very well
might be the cure to Alzheimer's disease."
"So much
Alzheimer's research has been done to look at amyloid-beta and tau," Reddy
said. "But ours is the first paper to strongly demonstrate that yes, there
is an amyloid-beta/phosphorylated tau interaction. And that interaction might
be causing the synaptic damage and cognitive decline in persons with
Alzheimer's disease."
Reddy and his lab
are already working on the next crucial questions. One is to define the binding
site or sites and exactly where within the neuron the interaction of amyloid-beta
and tau first occurs. The second is to find a way to inhibit that interaction
-- and thus maybe prevent or slow the progression of Alzheimer's.
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