|Quenching the flames of inflammatory brain aging|
By Dale Kiefer
Natural agents block the brain’s dual inflammatory pathways, improve circulation and restore acetylcholine. Clearly, any steps that can be taken to prevent cognitive decline – often viewed as the first step on the path to full- blown dementia – are well worth investigating.1
That’s why scientists around the world are intensively researching every aspect of the diseases associated with age-related dementia. Unfortunately, Alzheimer’s disease, once it takes hold, has no known cure. But some scientists believe that it may be possible to prevent the disease from ever starting.2 Although the exact causes of these dementias are not fully understood, there is reason for hope. Recent research has focused on some likely culprits and the natural agents that block them. Some of these agents treat symptoms of cognitive decline and early dementia. But the best news is that some of them may well provide a measure of prevention as well. While exact causes of some dementias remain elusive, the prevailing hypotheses hold that several factors may play a role in age-related neurodegeneration. It’s believed that toxins - byproducts of cellular metabolism - accumulate within cellular structures, causing eventual damage. Interruptions in cerebral blood flow are also suspect. Furthermore, it’s believed that inflammation plays a key role in triggering a cascade of events which eventually leads to the destruction of functional tissue.3 Elevation of a blood marker of chronic inflammation known as C-reactive protein increases stroke risk two to three fold.4
Some of the cells that are lost as a result of this neurodegenerative cascade include cells of the cholinergic system. Their loss leads to a decline in levels of a vital messenger chemical called acetylcholine, a neurotransmitter responsible for important functions such as memory, sleep and cognition. In Alzheimer’s disease, it’s well established that the presence of a protein, beta-amyloid (Aß), triggers inflammation.5 Early on, this inflammation and cholinergic dysfunction may be experienced as mild memory impairment or confusion.6 But left unchecked, it invariably leads to advancing cognitive decline, dementia and eventual death. Vascular dementia, most commonly caused by stroke, was once believed to be altogether different from Alzheimer’s-type dementia. But recently scientists have postulated that vascular dementia may share common elements of its pathology with Alzheimer’s, specifically, the disruption of normal cholinergic function, as mentioned above.7,8
Alpha GPC-acetylcholine precursor
GPC’s mechanism of action somewhat resembles that of the cholinesterase inhibitor drugs, such as donepezil (Aricept®) and rivastigmine (Exelon®), which are presently prescribed in this country to combat acetylcholine deficits among presumed Alzheimer’s and vascular dementia patients. Rather than interfering with a natural enzyme that breaks down acetylcholine, however, GPC provides a means for the body to manufacture new acetylcholine. This has a two-fold benefit. Normal neural transmission is restored, and cell membranes are left intact. When acetylcholine runs low, the body often raids stores of choline in the cell membranes in an effort to restore circulating acetylcholine to normal levels. In effect, the body is consuming itself, rendering cell membranes weak and potentially leading to nerve cell death. Please refer to Life Extension, July 2003, p.26 for a summary of GPC research.
Nexrutine®— nature’s COX-2 inhibitor
COX-2 is a villain. It is an intermediary enzyme: a link in a cascading chain of compounds which eventually trigger release of prostaglandins, resulting in inflammation. In Alzheimer’s disease this inflammatory damage spreads to neighboring cells in the brain. As they become inflamed they release stress chemicals in turn, which trigger more inflammation, setting into motion an accelerating spiral of decline.
Although scientists do not unanimously agree that halting inflammation may prevent the onset of Alzheimer’s and vascular dementia, many researchers continue to investigate the possibility. In one study on the effects of COX-2-inhibitor therapy, researchers concluded: “Our findings further support the importance of these disease-modifying drugs in the prevention and treatment of Alzheimer’s disease.”11 Other studies have also linked inflammatory processes with other neurodegenerative diseases, such as Lou Gehrig’s and Parkinson’s diseases.12,13