Alzheimer's disease (AD) is a progressive neurodegenerative disease that is the cause of 60–70% of cases of dementia affecting roughly 50 million people worldwide. AD is characterized by cognitive and memory dysfunction that is thought to result from the formation in the brain of both senile plaques containing amyloid-β (Aβ) and neurofibrillary tangles containing the microtubule-associated protein tau. The following understanding (A & B) on pathogenesis of AD has been found. A) There is a growing body of evidence which supports the hypothesis of faulty immune regulation and autoimmunity or inflammatory processes as viable mechanisms of the pathogenesis of Alzheimer's disease. High peripheral IL-6 secretion levels may be responsible for acute-phase proteins observed in the serum of AD patients. IL-1 levels are elevated in Alzheimer brain, and overexpression of IL-1 is associated with β-amyloid plaque progression. B) Additionally, oxidative stress is thought to be a key risk factor in the development of AD. Such stress is often triggered by reactive oxygen species such as the hydroxyl radical, superoxide anion, and hydrogen peroxide and is a typical activator of the JNK and p38 signaling pathways in AD. Tau is present in a hyperphosphorylated form in neurofibrillary tangles, with its phosphorylation having been shown to be mediated by several kinases including JNK, p38, and ERK. There is significant evidence showing that long-term daily meditation may be able to slow-down the neurodegenerative process of AD in crucial areas of the brain and result in beneficial changes in cortical thickness and gray matter volumes in the brain, thus reducing the risk of cognitive decline in Alzheimer's. Within the context of these recent findings A & B on the pathogenesis of AD, suggest a framework for the salutary effects of meditation on the disease progression in AD.
Alzheimer's disease (AD) is a progressive neurodegenerative disease that is the cause of 60–70% of cases of dementia affecting roughly 50 million people worldwide. AD is characterized by cognitive and memory dysfunction that is thought to result from the formation in the brain of both senile plaques containing amyloid-β (Aβ) and neurofibrillary tangles containing the microtubule-associated protein tau. The following understanding (A & B) on pathogenesis of AD has been found.
A) There is a growing body of evidence which supports the hypothesis of faulty immune regulation and autoimmunity or inflammatory processes as viable mechanisms of the pathogenesis of Alzheimer's disease. High peripheral IL-6 secretion levels may be responsible for acute-phase proteins observed in the serum of AD patients. IL-1 levels are elevated in Alzheimer brain, and overexpression of IL-1 is associated with β-amyloid plaque progression.
B) Additionally, oxidative stress is thought to be a key risk factor in the development of AD. Such stress is often triggered by reactive oxygen species such as the hydroxyl radical, superoxide anion, and hydrogen peroxide and is a typical activator of the JNK and p38 signaling pathways in AD. Tau is present in a hyperphosphorylated form in neurofibrillary tangles, with its phosphorylation having been shown to be mediated by several kinases including JNK, p38, and ERK.
There is significant evidence showing that long-term daily meditation may be able to slow-down the neurodegenerative process of AD in crucial areas of the brain and result in beneficial changes in cortical thickness and gray matter volumes in the brain, thus reducing the risk of cognitive decline in Alzheimer's. Within the context of these recent findings A & B on the pathogenesis of AD, suggest a framework for the salutary effects of meditation on the disease progression in AD.
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