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Could Alzheimer’s Be as Simple as Herpes Simplex?

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www.ProHealth.com • November 20, 2012


Article:
Intracerebral propagation of Alzheimer’s disease: Strengthening evidence of a herpes simplex virus etiology
– Source: Alzheimer’s & Dementia, Nov 16, 2012

By Melvyn J Ball, et al.

[Note: This fee-based article by researchers at Oregon Health & Science University in Portland reviews data supporting a list of reasons for pursuing their theory of how damage may spread in the Alzheimer’s brain via the HSV-1 virus known to produce most ‘cold sores’.] 

Abstract:
Background: A faulty human protein, abnormally phosphorylated tau, was recently publicized to spread “like a virus” from neuron to neuron in Alzheimer’s patients’ brains.

For several decades, we have been amassing arguments showing that herpes simplex virus type 1 (HSV-1), not p-tau, propagates this interneuronal, transsynaptic pathologic cascade.

Methods: We reiterate convincing data from our own (and other) laboratories, reviewing:

• The first anatomic foothold neurofibrillary tangles gain in brainstem and/or entorhinal cortex;

• The chronic immunosurveillance cellularity of the trigeminal ganglia wherein HSV-1 awakens from latency to reactivate;

• The inabilities of p-tau protein's physical properties to promote it to jump synapses;

• The amino acid homology between human p-tau and VP22, a key target for phosphorylation by HSV serine/threonine–protein kinase UL13;

• And the exosomic secretion of HSV-1–infected cells’ L-particles, attesting to the cell-to-cell passage of microRNAs of herpesviruses.

Results:
The now-maturing construct that reactivated HSV-1 best accounts for the intracerebral propagation of AD changes in the human brain should at last seem highly attractive.

This hypothesis might even explain statins' apparent mechanism in some studies for lowering AD incidence.

Conclusion: Provided that funding agencies will quickly ignite a new realm of investigation, the rejuvenated enthusiasm for testing this optimistic construct holds incalculable potential for:

• Rapid, efficacious clinical application,

• Through already available and relatively safe antiviral therapeutics.

Source: Alzheimer’s & Dementia, Nov 16, 2012. PMID:23159044, by Ball MJ, Lukiw WJ, Kammerman EM, Hill JM. Departments of Pathology and Neurology, Oregon Health & Science University, Portland, Oregon, USA. [Email: ballm@ohsu.edu]




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