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'Alzheimer's Protein' Seems to Slow Down Neurotransmitter Production
Posted: Tuesday, August 21, 2012 8:34 PM
Joined: 12/6/2011
Posts: 3326

From Alzheimer's Daily News:

(Source: Science Codex) - How abnormal protein deposits in the brains of Alzheimer's patients disrupt the signaling between nerve cells has now been reported by researchers in Bochum and Munich.

The scientists varied the amount of APP protein and related proteins associated with Alzheimer's disease in cell cultures, and then analyzed how this manipulation affected other proteins in the cell. The result: the amount of APP present was related to the amount of an enzyme that is essential for the production of neurotransmitters and therefore for communication amongst nerve cells.

"Our results point to a new mechanism by which the defective cleavage of the APP protein in Alzheimer's disease could be directly related to altered neurotransmitter production", reported Dr. Thorsten Müller from the Medizinisches Proteom-Center of the Ruhr-Universität. "As a result, the signal transduction of nerve cells could be disrupted, which, over an extended period, could possibly also cause the death of cells."

Lane Simonian
Posted: Wednesday, August 22, 2012 9:51 AM
Joined: 12/12/2011
Posts: 5140

There is a very interesting evolution on thinking regarding Alzheimer's disease.  The thinking goes something like this: all the drugs designed to remove amyloid plaques have failed so far.  Yet, a gene that is directly linked to increased abnormal processing of the amyloid precursor protein always causes Alzheimer's disease.  Moreover, one can see damage to a person's brain even before the production of the plaques.  Therefore Alzheimer's disease must be the result of  high levels of the amyloid precursor protein and not the amyloid plaques. 


The traps of this disease are many and this is just one of them. The true culprit in Alzheimer's disease is peroxynitrite.  It has been linked to every major feature of the disease.  The formation of peroxynitrites requires the activation of protein kinase C.  The formation of the amyloid precursor protein and amyloid plaques requires the activation of protein kinase C plus the release of intracellular calcium.  The latter takes more time.  Thus, the initial damage in Alzheimer's disease begins even before the production of the amyloid precursor protein and the production of amyloid plaque (the loss of smell, for instance).  Amyloid plaques do increase peroxynitrite levels but even if you could remove all the plaques the damage done by peroxynitrites would remain.  The only effective way to treat this disease is with peroxynitrite scavengers that are highly concentrated and can directly reach the brain (yeah, essential oils via aromatherapy).  This article provides further evidence for this theory of Alzheimer's disease. 


Furthermore, conditioned media derived from CT105-treated astrocytes enhanced neurotoxicity and pretreatment with NO and peroxynitrite scavengers attenuated its toxicity. These suggest that CT-APP may participate in Alzheimer's pathogenesis through MAPKs- and NF-κB-dependent astrocytosis and iNOS induction.