Concussionology® - Master The Complex
Research More Info 2
In 4 Hours It Looks Like Alzheimer's Disease
Comment by Dr. Mladenoff
One of the most amazing things that happens when you get a bonk on the head is that within a few brief hours your brain starts creating the chemical and cellular reaction that is identical to Alzheimer's Disease. The problem is that the 5 most dangerous words in the English language: "Maybe It Will Go Away" determines how you will respond to this slow downward spiral to mental and physical demise.
If you do nothing, it does not go away!
Are you on the fast tract to brain degeneration?
The key take away is that the absence of symptoms is not a reflection of this cellular reaction. Axons may be damaged and a rapid disturbed balance between amyloid B plaque genesis and catabolism following mTBI may be occurring.
One of the most amazing things that happens when you get a bonk on the head is that within a few brief hours your brain starts creating the chemical and cellular reaction that is identical to Alzheimer's Disease. The problem is that the 5 most dangerous words in the English language: "Maybe It Will Go Away" determines how you will respond to this slow downward spiral to mental and physical demise.
If you do nothing, it does not go away!
Are you on the fast tract to brain degeneration?
The key take away is that the absence of symptoms is not a reflection of this cellular reaction. Axons may be damaged and a rapid disturbed balance between amyloid B plaque genesis and catabolism following mTBI may be occurring.
Abstract:
Traumatic Brain Injury and Amyloid-B Pathology: A link to Alzheimer’s disease? Nat Rev Neurosci. 2010 May:11(5):361-370. Johnson VE, Stewart W, Smith DH.
Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI and the development of Alzheimer's disease (AD) later in life has been demonstrated, and it has been shown that amyloid-β (Aβ) plaques — one of the hallmarks of AD — may be found in patients within hours following TBI. Here, we explore the mechanistic underpinnings of the link between TBI and AD, focusing on the hypothesis that rapid Aβ plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Aβ genesis and catabolism following TBI.