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Protein That Repairs Alzheimer's Brain Damage Identified

by VR Sreeraman on Sep 26 2009 12:10 PM

Scientists from University of Medicine and Dentistry of New Jersey have identified a protein that can repair brain damage in Alzheimer's patients.

Scientists from University of Medicine and Dentistry of New Jersey have identified a protein that can repair brain damage in Alzheimer's patients.

They said that a protein called vimentin normally appears twice in a lifetime - when neurons in the brain are forming during the first years of life and, years later when the brain's neurons are under siege from Alzheimer's or other neurodegenerative diseases.

"Vimentin is expressed by neurons in regions of the brain where there is Alzheimer's damage but not in undamaged areas of the brain," said Dr Robert Nagele, a professor at UMDNJ and the study's corresponding author.

"When the patient shows up at the doctor's office with symptoms of cognitive impairment, the neurons have reached the point where they can no longer keep pace with the ever-increasing damage caused by Alzheimer's," he added.

While explaining the study results, Nagele likened neurons to a tree with long strands called dendrites branching off from the main part of the cell.

The dendrite branches are covered with 10,000 tiny "leaves" called synapses that allow neurons to communicate with each other. Vimentin is an essential protein for building the dendrite branches that support the synapses.

"A hallmark of Alzheimer's is the accumulation of amyloid deposits that gradually destroy the synapses and cause the collapse of dendrite branches," he said.

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"When the dendrites and synapses degenerate, the neuron releases vimentin in an attempt to re-grow the dendrite tree branches and synapses. It's a rerun of the embryonic program that allowed the brain to develop in the early years of life," Nagele added.

The researchers also reported some initial findings that indicated a similar damage response mechanism takes place following traumatic brain injury, suggesting the possibility that similar therapeutic agents could be developed to enhance repair both for sudden brain trauma and for progressive neurodegenerative diseases.

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The findings are published in journal Brain Research.

Source-ANI
SRM


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