PAIN RELIEF CENTER PAKISTAN

Sunday, March 7, 2010

Link Between Herpes Simplex Virus and Alzheimer’s Disease

Potential Role of Coriolus Vesicular supplementation. Herpes exists in two common forms. The majority of the population acquires Herpes Simplex Virus (HSV-1) during childhood from non sexual contact. Herpes Simplex Virus 2 (HSV-2) also known as genital herpes, is transmitted by sexual contact.

In 2000 , researchers led by Dr.Frank M Lafera at the Department of Neurology and Behavior at the University of California, Irvine, demonstrated that a synthetic protein that resembles the herpes simplex virus(HSV-1) mimics the structure and function of a protein call B-amyloid , a toxic agent that accumulates in the brains of Alzheimer patients.
Genetic sequencing revealed that two thirds a portion of the viral protein is identical to the beta-amyloid. The researcher showed that like B-amyloid, it could kill brain neurons, a key feature in Alzheimer’s. Moreover, in laboratory experiments, the viral protein formed abnormal twisted fibers like those found in brains of Alzheimer’s patients the definitive hallmark of diseases.
According to Dr.Laferla most people are exposed to HSV-1 , but do not develop Alzheimer’s ,however, recent studies show that people genetically disposed to Alzheimer’s, are more likely to develop the disease if they are exposed to herpes.
In December 2008,Professor Ruth Itzhaki and her team at Manchester University ‘ s faculty of life sciences published in the journal of pathology that the HSV-1 DNA is located very specifically in amyloid plaques :90% of plaques in Alzheimer’s disease suffers brains contain HSV-1 DNA and most of the viral DNA is located with in amyloid plaques.
The team had previously shown that HSV-1 infection of nerve –type cells induces deposition of the main component, B-amyloid, of amyloid plaques.
Together these findings strongly implicate HSV-1 as a major factor in the information of amyloid deposits and plaques, abnormalities through by many in the fields to be major contributors of Alzheimer’s. This finding is a reconfirmation of Dr.Laferrla;s previous work In 2000.
The University of Manchester’s data strongly suggest that HSV-1 has a major role in Alzheimer’s disease and point to in preliminary experiments they have shown that acyclovir reduces the amyloid depositions and also reduces certain other features of the disease which they have found are caused by HSV-1 infection. Further research is going on potential use of acyclovir as therapeutic agent for the treatment of Alzheimer’s disease.
For those patients who are not able to tolerate the side effects of acyclovir treatment, the evidence that Coriolus vesicular supplementation reduces viral loads in both chronic Fatigue Syndrome patients and in HPV (LSIL) patients may have applications in neurodegenerative diseases in which viral infection plays a role.


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