Best not read if you aren't into technoblurb

In my "old life", I did a lot of research on Alzheimers disease. The current "schtick" about the cause of ALZ still implicates the formation of "plaques and tangles made out of "beta folded sheets" of a 41-42(?) amino acid chain called beta protein, which is just a small peptide cut from a larger transmembrane protein called beta precursor protein. Like alpha synuclein, if it doesn't fold into Beta sheets, it can be eliminated from the body. If it does fold into the very configurationally stable sheets, it can't be eliminated and builds up because, once it forms a sheet, others of its kind are then more eisily "crystallized" epitaxiallly to form the gummed up plaque and tangles that are the undoing of a neuron because this "junk" chokes off neuronal axons and thus kills the cellular functions and the cells die off.
Well, it's a long shot, but serotonergic neurons are present in the cerebral cortex as are a lot of serotonergic axons projecting into the cortex. Serotonin is just 5-hydroxytryptamine, derived from tryptophan (an indole amino acid found in most foods), and, if enzymatically turned into 5,6-dihydroxytrypamine, this is closely related to the Dopamine oxidative cytotoxic 5,6- dihydroxyindole discussed above. You see what i'm getting at? If serotonergic neurons also try to protect 5HT from oxidation and get killed off by producing and using alpha synuclein, then get rid of alpha synuclein protein (a by-product of the vesicles that hold or protect 5-HT neurotransmitter from leaking out into the cytosol where oxidative processes occur) and alpha synuclein is ejected from the cell and misfolds into junk plaques (also found in ALZ patients brains), then the reason why cortical neurons produce beta protein is because the cortical neuron is put in "apoptotic mode" because the serotonergic neurons are dying. Since serotonergic neurons no longer ennervate cortical neurons, then a lot of beta protein is formed as a result of "clipping of the beta precursor protein as part of getting rid of the dying cell.
Thus, protection of serotoneric neurons by stopping the misfolding of alpha synuclein by product, may help protect cortical neurons from dying and clogging up the cortex with plaques and tangles formed by beta protein, which just keeps on forming and killing more cortical neurons. IN essence a cascade effect caused by other junk proteins far from the actual cortical neurons.
I may be dreaming, but that is what science is all about; to think of possibilities and then prove them wrong or right. cs