Washington: In what could pave the way for effective therapies for Alzheimer`s, scientists claim to have discovered a protein which plays a key role at a cellular
level in the development of the disease.
An international team, led by Prof Jrgen Gtz and Dr Lars Ittner of University of Sydney, has revealed how a protein called TAU affects and mediates toxicity of amyloid-b, which together with TAU causes the symptoms of Alzheimer`s.
According to Prof Gtz, this significant breakthrough has implications for how the disease develops and how it may be treated, the `Cell` journal reported.
"The main clinical feature of Alzheimer`s disease is a progressive loss of cognition, accompanied by aggression and mood disturbance, and eventually, the patients need to be
institutionalised. The toll of Alzheimer`s disease on patients and their families and caretakers is enormous. Unfortunately, to date Alzheimer`s disease is incurable.
"A handful of approved drugs provide if at all only very modest symptomatic relief, without curing the disease.
Therefore, to develop effective treatments, it is absolutely necessary that the basic mechanisms underlying these disorders be understood. This was our challenge," he said.
The brain of all Alzheimer`s patients is characterized by two types of insoluble deposits -- amyloid-b plaques and neurofibrillary tangles, the latter formed by the protein TAU.
In their research, the scientists found that TAU is essential for the positioning of yet another protein, the kinase FYN, at the dendritic site of the synapse, which then
renders the neuron vulnerable to amyloid-b.
"By genetically deleting TAU or introducing a non-functional variant of TAU, we found we could prevent the development of symptoms in mouse models of Alzheimer`s. These
mice showed normal survival and their memory appeared to be perfectly fine," Dr Ittner said.
In the second part of the research, the team explored the potential of their discovery for a treatment of Alzheimer`s disease.
"We translated our findings into a novel therapeutic approach by using a small peptide that mimics the effects of removing TAU from the synapse, and we were thrilled to see
that this not only fully prevented the pathology in our Alzheimer`s disease models but cleared their memory deficits," Dr Ittner said.
Added Prof Gtz: "Although there is still a long way to go we believe we may have found a way of treating Alzheimer`s."