Causes and possible treatments for hereditary movement disorder discovered by Einsteins scientific
Researchers at the Albert Einstein College of Medicine of Yeshiva University have discovered the underlying cause of a type of ataxia, hereditary diseases characterized by poor balance, loss of posture and difficulty performing rapid coordinated movement. A discovery that could lead to better treatments for the disease - their work, a drug that has significantly improved the motor coordination performed in mice with ataxia. The study appears in the March issue of Nature Neuroscience and was published in the advance online edition of the featured.Research by Dr. Kamran Khodakhah, associate professor of neuroscience at Einstein, a type of ataxia in a concentrated form called episodic ataxia type 2. The result of genetic mutations that affect calcium channels that are found
in the release of neurotransmitters in the brain and regulates the excitability of neurons involved. Episodic ataxia type 2 was thought to be due to a presumption of reduced transmission of neurotransmitters, but scientists Einstein that something was happening. They studied the specialized cells of the brain called the cerebellum Purkinje cells, which are rich in calcium channels.Purkinje cells help coordinate the movement to act as information centers: Support and other sensory stimuli transmitted to more than 150,000 entries synaptic excitation and inhibition, combined with the cellos own intrinsic activity or a pacemaker, then send the signals necessary for motor coordination.The researchers investigated whether ataxia might be a reduction of the intrinsic accuracy of
the Purkinje cells of the pacemaker. The study of a series of mouse models of ataxia type-2, found a loss of genes depends on the accuracy of the pacemaker in the Purkinje cells, prevents a fraction of its strength and timing of synaptic inputs to send signals from direction of muscle movement. The loss of accuracy due to the pacemaker is reduced activity of calcium-activated potassium channels in Purkinje cells - a direct Pages: [1] 2