QUESTION OF THE DAY

In the brain, there are NG2 cell that have still a potential differentiatiation to either oligodendrocytic or other glial cells.   That power to differentiate one way or the other must be exploited as differentiation decreases proliferation. A growth factor must be behind the push toward one specific direction of differentiation.  We need to specify which growth factor for which differentiation.   Another intriguing fact is that these cells appear to be located in only 2 locations, one of which is very close to blood vessel as if the may have or can be influence by VEGF.  we will be looking very closely into this.

Alzheimer dementia seems to be due to increase of Amyloid deposits.  The cause of this accumulation of Amyloid compound seems to involve either production which is favored when with aging there seems to be a decrease of phosphatase activity, leaving phosphorylation intact to involve the Amyloid product.  Phosphorylation and calcification involve microtubule entangling into Neurofibbrillary bundles that characterize the disease.  Is Methylation of genes prompting the initial event? 
there are 2 main roads to calcification, one by influx of calcium though the calcium channels, and the other through the APOE.  Do you believe blocking the APOE by gene intervention or though immune intervention will slow down Neurofibrillary formation and slow down the dementia process?

The 3rd intervention is of course boosting the scavenger who can clean up the mess created by the Amyloid
what is the equivalent of macrophages in the Brain again?

The Amyloid are found in the extra-cellular matrix through activity of Exosome, is there here an opportunity for intervention, let's look closely into the formation and activity of the exosome!