Head/Brain Injury

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"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The Children of Hurin
- Head/Brain Injury -

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Observations:

Sports Brain Trauma May Cause Disease Mimicking ALS, Researchers Find

ScienceDaily (Aug. 17, 2010) — New research by the Center for the Study of Traumatic Encephalopathy (CSTE) at Boston University School of Medicine (BUSM) and the Department of Veterans Affairs (VA) provides the first pathological evidence that repetitive head trauma experienced in collision sports is associated with motor neuron disease, a neurological condition that affects voluntary muscle movements. The most common form of motor neuron disease is amyotrophic lateral sclerosis (ALS) or Lou Gehrig's disease. The findings will be published in the September issue of the Journal of Neuropathology and Experimental Neurology... In this study, funded in part by an unrestricted gift from the National Football League (NFL) to the CSTE, McKee found that when they died, all 12 athletes showed neuropathological evidence of chronic traumatic encephalopathy (CTE), a progressive degenerative brain disease characterized by deposits of an abnormal form of tau protein and believed to be caused by repetitive head trauma. In the three athletes with motor neuron disease, abnormal tau protein deposits were not only found throughout the brain, but also in the spinal cord...
http://www.sciencedaily.com/releases/2010/08/100817134304.htm

Phytonutrients and Metabolic Stimulants as protection Against Neurodegeneration and Excitotoxicity
The Journal of the American Nutraceutical Association
January 2000 Vol. 2, No. 3 Pg. 30
With severe injuries to the brain the amount of glutamate in the extracellular space may reach levels 100X that normally seen.7,8 This can overwhelm the glutamate transporter system, resulting in prolonged activation of the glutamate receptor with a resultant excess calcium entry into the neuron. Normally, intracellular calcium is carefully regulated within the cell, either by extrusion from the cell or by trapping by the mitochondria or endoplasmic reticulum. In cases of cellular dysfunction, as seen with ischemia/hypoxia, hypoglycemia and neurodegenerative disorders, these homeostatic mechanism malfunctions lead to calcium accumulation intracellularly. Elevated levels of calcium can trigger activation of protein kinase C with subsequent expression of membrane bound phospholipase A2 triggering the release of arachidonic acid from the cell membrane. Arachidonic acid is then acted on by lipoxygenase and cyclooxygenase I and II, leading to the generation of leukotrienes and prostaglandins ( PGE2, PGD2 ). These eicosanoids are responsible for a cascade of inflammatory reactions that include the generation of reactive oxygen species and inflammatory cytokines ( IL-1ß,IL-6, TNF-alpha).11-12 These reactive oxygen species damage cellular proteins ( protein carbonyl products), DNA and lipids ( lipid peroxidation). Intracellular calcium also induces and activates nitric oxide synthease ( NOS) which, when overactive, can lead to the formation of the powerful nitrogen radical peroxynitrite formed from a reaction of nitric oxide with the superoxide radical.13 Peroxynitrite can enter the mitochondria and damage the electron transport enzymes, especially complex I and IV, leading to impaired energy production by the mitochondria, making the neuron infinitely more susceptible to excitotoxicity The generation of increased levels of free radicals within the cell, if intense enough, can activate the p53 tumor suppressor gene triggering apoptosis.14 Excess glutamate can also kill neurons by necrosis as well.
http://www.ana-jana.org/Journal/journals/JANAVol23.pdf

Can head injury cause motor neuron disease?
Neurology Now:
November/December 2010 - Volume 6 - Issue 6 - p 11–13
doi: 10.1097/01.NNN.0000392627.15551.f6
Departments: The Waiting Room

http://journals.lww.com/neurologynow/Fulltext/2010/06060/Can_head_injury_cause_motor_neuron_disease_.4.aspx

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Known sources:

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Natural sources:

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References:

[The tobacco plant extract anatabine is also thought to be a strong anti-inflammatory. It has also been shown in mouse studies to reverse AD. But, mice are not men. Still… might it be inhibiting the same processes?]

New Drug Could Treat Alzheimer's, Multiple Sclerosis and Brain Injury
ScienceDaily (July 24, 2012) — A new class of drug developed at Northwestern University Feinberg School of Medicine shows early promise of being a one-size-fits-all therapy for Alzheimer's disease, Parkinson's disease, multiple sclerosis and traumatic brain injury by reducing inflammation in the brain… By addressing brain inflammation, the new class of drugs -- represented by MW151 and MW189 -- offers an entirely different therapeutic approach to Alzheimer's than current ones being tested… MW151 and MW189 work by preventing the damaging overproduction of brain proteins called proinflammatory cytokines…
http://www.sciencedaily.com/releases/2012/07/120724171302.htm
http://www.eurekalert.org/pub_releases/2012-07/nu-ndc072312.php
[No PubMed citation yet]

How a Single Brain Trauma May Lead to Alzheimer's Disease
ScienceDaily (July 24, 2012) — A study, performed in mice and utilizing post-mortem samples of brains from patients with Alzheimer's disease, found that a single event of a moderate-to-severe traumatic brain injury (TBI) can disrupt proteins that regulate an enzyme associated with Alzheimer's. The paper, published in The Journal of Neuroscience, identifies the complex mechanisms that result in a rapid and robust post-injury elevation of the enzyme, BACE1, in the brain… "A moderate-to-severe TBI, or head trauma, is one of the strongest environmental risk factors for Alzheimer's disease. A serious TBI can lead to a dysfunction in the regulation of the enzyme BACE1. Elevations of this enzyme cause elevated levels of amyloid-beta, the key component of brain plaques…”
http://www.sciencedaily.com/releases/2012/07/120724171227.htm
http://www.newswise.com/articles/new-research-determines-how-a-single-brain-trauma-may-lead-to-alzheimer-s-disease

Depletion of GGA1 and GGA3 mediates post-injury elevation of BACE1.
Walker KR, Kang EL, Whalen MJ, Shen Y, Tesco G.
The Journal of Neuroscience, July 25, 2012 DOI: 10.1523/JNEUROSCI.5491-11.2012
[No PubMed citation yet]

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