New target for drug discovery for Alzheimer's.
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Researchers at the University of Pennsylvania School of Medicine have shown that impaired function and loss of synapses in the hippocampus of a mouse form of Alzheimer's disease (AD) is related to the activation of immune cells called microglia, which cause inflammation. These events precede the formation of tangles - twisted fibers of tau protein that build up inside nerve cells - a hallmark of advanced AD. The researchers report their findings in the February 1 issue of Neuron. "Abolishing the inflammation caused by the accumulation of the tau protein might be a new therapy for treating neurodegenerative disorders," says senior author Virginia Lee, PhD, Director of the Center for Neurodegenerative Disease Research. "This work points the way to a new class of drugs for these diseases."
In Alzheimer's and other neurodegenerative diseases, misfolded tau and other proteins accumulate inside neurons. Proteins used to make healthy synapses are moved via microtubules to the synapse along the nerve axon. However, accumulation of tau in clumps inside nerve cells (that is, the tangles described 100 years ago by Alzheimer in the first reported AD patient) impairs the function of nerve cells and causes them to degenerate. This is because tau is needed to stabilize microtubules like cross-ties stabilize train tracks. But if tau clumps, the microtubules break up, thereby disrupting the transportation network in normal nerve cells. This has lethal consequences because nerve-cell axons and dendrites are critically dependent on this normal transportation network.
The misfolded tau proteins aggregate and form sheets called fibrils that accumulate in different parts of the brain. The resulting impaired axonal transport of proteins and other cargoes needed to maintain synapses can cause nerve-cell loss, with subsequent dementia, parkinsonism, or weakened motor skills in peripheral muscles, and later muscle atrophy. Hence, blocking fibril formation or eliminating misfolded proteins have become targets for drug discovery for Alzheimer's, Parkinson's, and related disorders.
Alzheimer's Donation
Donate Online Now
.
Researchers at the University of Pennsylvania School of Medicine have shown that impaired function and loss of synapses in the hippocampus of a mouse form of Alzheimer's disease (AD) is related to the activation of immune cells called microglia, which cause inflammation. These events precede the formation of tangles - twisted fibers of tau protein that build up inside nerve cells - a hallmark of advanced AD. The researchers report their findings in the February 1 issue of Neuron. "Abolishing the inflammation caused by the accumulation of the tau protein might be a new therapy for treating neurodegenerative disorders," says senior author Virginia Lee, PhD, Director of the Center for Neurodegenerative Disease Research. "This work points the way to a new class of drugs for these diseases."
In Alzheimer's and other neurodegenerative diseases, misfolded tau and other proteins accumulate inside neurons. Proteins used to make healthy synapses are moved via microtubules to the synapse along the nerve axon. However, accumulation of tau in clumps inside nerve cells (that is, the tangles described 100 years ago by Alzheimer in the first reported AD patient) impairs the function of nerve cells and causes them to degenerate. This is because tau is needed to stabilize microtubules like cross-ties stabilize train tracks. But if tau clumps, the microtubules break up, thereby disrupting the transportation network in normal nerve cells. This has lethal consequences because nerve-cell axons and dendrites are critically dependent on this normal transportation network.
The misfolded tau proteins aggregate and form sheets called fibrils that accumulate in different parts of the brain. The resulting impaired axonal transport of proteins and other cargoes needed to maintain synapses can cause nerve-cell loss, with subsequent dementia, parkinsonism, or weakened motor skills in peripheral muscles, and later muscle atrophy. Hence, blocking fibril formation or eliminating misfolded proteins have become targets for drug discovery for Alzheimer's, Parkinson's, and related disorders.
posted by Valery Yermalitsky at
6:39 AM
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