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New Path for Novel Alzheimer's Therapies

May 22, 2010 — Researchers from the University of the Basque Country (UPV/EHU) have found a new Alzheimer's-related mechanism that could give rise to the development of new therapies against this disease.


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The study was recently published in the journal Cell Calcium, and the authors have already applied for a European patent to protect the commercial exploitation of this new discovery.

The novelty lies in a new mechanism through which the amyloid peptide, the major pathogen in Alzheimer's disease, provokes neuronal death. The Basque researchers have found that this peptide activates some receptors that lead cells to overexcitation and subsequent death; when such receptors are blocked with specific drugs, neurons are protected from the peptide-related lethal effects. This finding is particularly relevant for the development of new therapies slowing down Alzheimer's progression.

The research work was supervised by Dr. Carlos Matute, Director of Neurotek research centre and Head of the Neurobiology Laboratory of the Neurosciences Department at the University of the Basque Country (UPV/EHU). The research team led by Dr. Matute deals with the molecular and cell fundamentals of neurodegenerative diseases such as Alzheimer's or multiple sclerosis. In particular, it focuses on the mechanism leading to cell death in the nervous system by using different tests based on cell cultures, experimental animals, human brains coming from demised people suffering these diseases and living patients' samples.

This team, which has already released many patents, also searches for markers supporting early diagnosis of these diseases.

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The above story is reprinted from materials provided by Elhuyar Fundazioa.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Elena Alberdi, Mª Victoria Sánchez-Gómez, Fabio Cavaliere, Alberto Pérez-Samartín, José Luis Zugaza, Ramón Trullas, María Domercq, Carlos Matute. Amyloid β oligomers induce Ca2+ dysregulation and neuronal death through activation of ionotropic glutamate receptors. Cell Calcium, 2010; 47 (3): 264 DOI: 10.1016/j.ceca.2009.12.010
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