A number of interesting new directions in Alzheimer's research have been emerging over the past few years. There's the choroid plexus connection, and the possibility of repairing the normal mechanisms of amyloid removal, for one. It turns out that amyloid creation and removal are actually very rapid, dynamic processes, and the buildup towards Alzheimer's is a slowly growing imbalance between ongoing creation and removal. Also, the realization that Alzheimer's looks an awful lot like type 2 diabetes at a biochemical level, with all the same lifestyle risk factors relating to exercise, eating and visceral fat. Lastly for this list, there is some form of biochemical connection between Alzheimer's and the inflammatory immune response.
Chronic inflammation crops up everywhere you look in the pathology of aging, and as a risk factor for all the common age-related diseases. More chronic inflammation isn't a good thing, but an age-damaged immune system will give you more of it whether you want it or not. Excess visceral fat will add even more inflammation on top of that.
The latest Alzheimer's science to catch my eye springs from research into inflammation and amyloid plaques, but turns up a result that looks a lot like immune therapy:
Earlier studies had shown that Alzheimer's patients tend to have elevated amounts of TGF-β, which plays a key role in activating immune system response to injury. Some had thought the presence of the molecule was simply an attempt to quiet the inflammatory response caused by a buildup of plaque.
Instead, the team found that as much as 90 percent of the plaques were eliminated from the brains of mice genetically engineered to block TGF-β in the peripheral immune cells.
Amyloid plaques are thought to damage brain nerve cells (neurons) and stimulate a response in nearby inflammatory cells called microglia. Theoretically, Alzheimer's might be treated by somehow preventing or removing the plaque buildup and calming the inflammation.
When TGF-β was blocked, the immune system seemed to unleash immune cells known as peripheral macrophages. The macrophages passed through the blood-brain barrier and surrounded the neurons and plaques in the brains of mice. "If results from our study in mice engineered to develop Alzheimer's-like dementia are supported by studies in humans, we may be able to develop a drug that could be introduced into the bloodstream to cause peripheral immune cells to target the amyloid plaques."
This wasn't the result researchers were expecting when they engineered these mice. So much of progress comes about through unintentional discoveries in the course of sensible exploration.