Neuronal activity induces tau release from healthy neurons

Public release date: 15-Feb-2013
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Contact: Barry Whyte
communications@embo.org
49-622-188-91108
European Molecular Biology Organization

HEIDELBERG, 15 February 2013 Researchers from King's College London have discovered that neuronal activity can stimulate tau release from healthy neurons in the absence of cell death. The results published by Diane Hanger and her colleagues in EMBO reports show that treatment of neurons with known biological signaling molecules increases the release of tau into the culture medi-um. The release of tau from cortical neurons is therefore a physiological process that can be regulated by neuronal activity.

Tau proteins stabilize microtubules, the long threads of polymers that help to maintain the structure of the cell. However, in Alzheimer's disease or certain types of dementia, tau accumulates in neurons or glial cells, where it contributes to neurodegeneration.

In addition to intracellular aggregation, recent experiments have shown that tau is released from neuronal cells and taken up by neighboring cells, which allows the spread of aggregated tau across the brain. This release could occur passive-ly from dying neuronal cells, though some evidence suggests it might take place before neuronal cell death and neurodegeneration. The new findings indicate that tau release is an active process in healthy neurons and this could be altered in diseased brains.

"Our findings suggest that altered tau release is likely to occur in response to changes in neuronal excitability in the Alzheimer's brain. Secreted tau could therefore be involved in the propagation of tau pathology in tauopathies, a group of neurodegenerative diseases associated with the accumulation of tau proteins in the brain," commented Diane Hanger, Reader in the Department of Neuroscience at King's College London. In these experiments, Amy Pooler, the lead au-thor, revealed that molecules such as potassium chloride, glutamate or an AM-PA receptor agonist could release tau from cortical neurons in an active physio-logical process that is, at least partially, dependent on pre-synaptic vesicle se-cretion.

The new findings by the scientists indicate that tau has previously unknown roles in biological signaling between cells, in addition to its well-established role in stabilizing microtubules.

"We believe that targeting the release of tau could be explored as a new thera-peutic approach for the treatment of Alzheimer's disease and related tauopa-thies," said Hanger. Additional studies are needed in model organisms to test this hypothesis further.

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Physiological release of endogenous tau is stimulated by neuronal activity
Amy M Pooler, Emma C Phillips, Dawn HW Lau, Wendy Noble, Diane P Hanger

Read the paper:

doi: 10.1038/embor.2013.15
http://www.nature.com/embor/journal/vaop/ncurrent/full/embor201315a.html

Further information on EMBO reports is available at http://www.nature.com/embor

Media Contacts

Barry Whyte
Head | Public Relations and Communications

Barbara Pauly
Editor
Tel: 49-6221-8891-109
pauly@embo.org

About EMBO

EMBO is an organization of more than 1500 leading researchers that promotes excellence in the life sciences. The major goals of the organization are to sup-port talented researchers at all stages of their careers, stimulate the exchange of scientific information, and help build a European research environment where scientists can achieve their best work.

EMBO helps young scientists to advance their research, promote their interna-tional reputations and ensure their mobility. Courses, workshops, conferences and scientific journals disseminate the latest research and offer training in tech-niques to maintain high standards of excellence in research practice. EMBO helps to shape science and research policy by seeking input and feedback from our community and by following closely the trends in science in Europe.

For more information: www.embo.org

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Public release date: 15-Feb-2013
[ | E-mail | Share ]

Contact: Barry Whyte
communications@embo.org
49-622-188-91108
European Molecular Biology Organization

HEIDELBERG, 15 February 2013 Researchers from King's College London have discovered that neuronal activity can stimulate tau release from healthy neurons in the absence of cell death. The results published by Diane Hanger and her colleagues in EMBO reports show that treatment of neurons with known biological signaling molecules increases the release of tau into the culture medi-um. The release of tau from cortical neurons is therefore a physiological process that can be regulated by neuronal activity.

Tau proteins stabilize microtubules, the long threads of polymers that help to maintain the structure of the cell. However, in Alzheimer's disease or certain types of dementia, tau accumulates in neurons or glial cells, where it contributes to neurodegeneration.

In addition to intracellular aggregation, recent experiments have shown that tau is released from neuronal cells and taken up by neighboring cells, which allows the spread of aggregated tau across the brain. This release could occur passive-ly from dying neuronal cells, though some evidence suggests it might take place before neuronal cell death and neurodegeneration. The new findings indicate that tau release is an active process in healthy neurons and this could be altered in diseased brains.

"Our findings suggest that altered tau release is likely to occur in response to changes in neuronal excitability in the Alzheimer's brain. Secreted tau could therefore be involved in the propagation of tau pathology in tauopathies, a group of neurodegenerative diseases associated with the accumulation of tau proteins in the brain," commented Diane Hanger, Reader in the Department of Neuroscience at King's College London. In these experiments, Amy Pooler, the lead au-thor, revealed that molecules such as potassium chloride, glutamate or an AM-PA receptor agonist could release tau from cortical neurons in an active physio-logical process that is, at least partially, dependent on pre-synaptic vesicle se-cretion.

The new findings by the scientists indicate that tau has previously unknown roles in biological signaling between cells, in addition to its well-established role in stabilizing microtubules.

"We believe that targeting the release of tau could be explored as a new thera-peutic approach for the treatment of Alzheimer's disease and related tauopa-thies," said Hanger. Additional studies are needed in model organisms to test this hypothesis further.

###

Physiological release of endogenous tau is stimulated by neuronal activity
Amy M Pooler, Emma C Phillips, Dawn HW Lau, Wendy Noble, Diane P Hanger

Read the paper:

doi: 10.1038/embor.2013.15
http://www.nature.com/embor/journal/vaop/ncurrent/full/embor201315a.html

Further information on EMBO reports is available at http://www.nature.com/embor

Media Contacts

Barry Whyte
Head | Public Relations and Communications

Barbara Pauly
Editor
Tel: 49-6221-8891-109
pauly@embo.org

About EMBO

EMBO is an organization of more than 1500 leading researchers that promotes excellence in the life sciences. The major goals of the organization are to sup-port talented researchers at all stages of their careers, stimulate the exchange of scientific information, and help build a European research environment where scientists can achieve their best work.

EMBO helps young scientists to advance their research, promote their interna-tional reputations and ensure their mobility. Courses, workshops, conferences and scientific journals disseminate the latest research and offer training in tech-niques to maintain high standards of excellence in research practice. EMBO helps to shape science and research policy by seeking input and feedback from our community and by following closely the trends in science in Europe.

For more information: www.embo.org

---

[ | E-mail | Share ]

?

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-02/embo-nai021513.php

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