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PRE-INFECTION. “The normal protein that becomes a prion has either alpha helixes or disordered structure. This shape is found in most cells and does not cause any damage.” https://lnkd.in/dKV3Xez View in LinkedIn

MOLECULAR VARIANTS. “Prion proteins can exist in multiple structures called conformers. These different shapes are created by sigma bonds in their chemical structures that allow the rotation of parts of the protein.” https://lnkd.in/dKV3Xez View in LinkedIn

THE SWITCH. “When the PrP becomes a prion its normal function stops. It is possible that it is this loss of normal function that causes some of the damage in prion diseases, not just the accumulation of the clumped proteins.” https://lnkd.in/dKV3Xez View in LinkedIn

NON-INFECTIOUS NORMAL PROTEIN. “The prion protein is known as PrP before it becomes the pathogen PrPsc. PrP has many different normal important physiological roles. PrP is involved in maintaining myelin formation, development of T cells and is critical in stem cells that make blood cells and M cells of the intestine immune centers. PrP is involved in virus reproduction and modulation of inflammation in the CNS.” https://lnkd.in/dKV3Xez View in LinkedIn

SEDITIOUS PROTEIN. “The basic protein that becomes a prion has multiple important normal roles in cells, particularly in immune cells. Also, the immune system is now known to be critical to its spread. A simple protein that has only “self” antigens falls beneath the cracks of the immune surveillance system. In fact, it can create prion crystals in the immune system. Like a virus, it hijacks components of the immune system and rides along with immune cells into the central nervous system.” https://lnkd.in/dKV3Xez View in LinkedIn

COPPER HYPOTHESIS. “Copper exposure has been linked to prion pathogenesis. Our study establishes a direct link, at the molecular level, between copper exposure and PrP neurotoxicity.” https://lnkd.in/dy7nHgK View in LinkedIn

PATHWAYS. “Prions introduced through surgery can spread from the eye along visual pathways. Spread can occur along the vagus nerve to medulla, pons, midbrain. In transplants for treatment of Parksinson’s, the new neurons develop the same disease from the local cells. Injection of abnormal amyloid beta, tau and alpha synuclein in animal experiments shows spread into the new brain.” https://lnkd.in/dKV3Xez View in LinkedIn

INFECTIOUS HIGHWAY. “All of these prion like proteins appear to spread along brain circuits. Tau is known to start in the entorhinal region near the nose spreading to entorhinal cortex along glutamate neurons, then to hippocampus, amygdala and neocortex.” https://lnkd.in/dKV3Xez View in LinkedIn

TRAVELING PROTEIN. “Recently, it has been discovered that tau can be released from neurons and taken up by the next neuron. Alpha synuclein can also be transmitted out of a neuron in vesicles, enter another cell, and then when inside the cell break out of the vesicle disrupting the mitochondria.” https://lnkd.in/dKV3Xez View in LinkedIn

PRION-LIKE DISEASES. “Five critical molecules have been studied in this regard—amyloid and tau in Alzheimer’s, alpha-synuclein in Parkinson’s, SOD1 in ALS, and polyglutamine in Huntington’s. Just like PrP each have normal functions in the brain and, then, when misfolded, become prions. It appears that amyloid beta, tau and alph-synuclein influence each other in Alzheimer’s and Parkinson’s.” https://lnkd.in/dKV3Xez View in LinkedIn