Saturday, November 12, 2011

Alzheimer’s disease and Calcium signaling:

After studying the neurophysiology chapters, it came to my attention the degenerative and progressive brain disease known as Alzheimer’s disease (AD). President Obama signed the National Alzheimer's Plan into a law: this law is working in the creation of funding research for stem cell therapy, early detection, prevention, treatment, and care as well as to reduce the financial impact for the families with AD.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder. Risk factors included; history of a family member that has/had the disease, advancing age and a combination of gene mutation and environmental factors. There are two types of AD; an early onset at age 40 and a late onset at age 60. AD affects all the areas of the brain (language, memory, perception, emotional behavior, and cognitive skills) as the disease progresses it continues to reduce the function of all these brain areas. People with AD ultimately lose the ability to understand language, recognize family members and perform basic daily activities, and death. There is no cure for AD, there are drugs that only work to reduce and slow the symptoms and that social activities may reduce the onset of the disease in older adults. (1).

The intracellular role of Ca2+ is fundamental for proper neuronal function. Disruption of Ca2+ homeostasis leads to a serious neurodegenerative disorders such as AD. One of the main characteristics of AD is the excessive production of beta-amyloid (Aβ) and its accumulation, causes disruption of Ca2+ permeability, signaling which leads to detrimental effects on neurons such as amyloid plaques, neurofibrillary tangles and accumulation of amyloids in the brain and CSF. Calcium regulation in the cytosol depends on the receptor voltage gated Ca2+ channel in the endoplasmic reticulum and mitochondria. An increase in Ca2+ leads to excitation, synaptic degeneration and cell death. On the other hand, reduced levels of calcium act as a neuro-protective, defending the brain from neuronal injury and degradation. For that reason, research in Ca2+ signaling is important to reduce and block the increase of Ca 2+ permeability caused by Aβ (Demuro, 2010).

References:

(1). http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001767/

Angelo, Demuro; Ian Parker, and Grace E. Stutzmann. Calcium Signaling and Amyloid Toxicity in Alzheimer Disease. JBC Papers in Press. 2010. http://www.jbc.org/content/285/17/12463.full.pdf+html

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