|Inflammation and the aging brain|
By Dale Kiefer
Inflammation is now thought to play a role in pathological conditions ranging from anemia and allergy to coronary heart disease, psoriasis and even stroke. From inflamed gums that may contribute to cardiovascular disease, to playing a crucial role in fanning the flames of cancer cell growth, inflammation has been implicated in many more diseases than was previously believed.
Recently, inflammation has also been recognized as playing a central role in the debilitating cognitive decline that characterizes neurological disorders such as Alzheimer’s disease and vascular dementia. Although mental decline and memory loss have long been considered inevitable hallmarks of old age, new research suggests that such inflammation/age-associated decline is avoidable. Indeed, findings reported by some scientists suggest that early intervention in low-grade inflammation may offer some protection against these dreaded brain diseases.
The many guises of inflammation
But inflammation, including fever, serves a useful purpose in the body. Even sunburn is a result of the body’s attempt to repair damage inflicted by ultraviolet radiation. In fact, inflammation is an ingenious adaptation that allows the body to defend against clear and present dangers.
For instance, when virulent bacteria invade, they thrive precisely at the body’s normal temperature of 98.6 ºF (37 ºC). Once established, they pour toxins into the bloodstream, while continuing to proliferate exponentially. The immune system mounts a defense, but cellular defenders may be thwarted or simply overwhelmed. In response, the body turns up the furnace. Sensitive to the slightest temperature increases, pathogens perish. The body wins the battle. Fever breaks and all is well.
This is just one example of inflammation’s beneficial nature. But some inflammation goes too far. Fever doesn’t always vanquish the invading horde and fade back to a state of disease-free normalcy. Occasionally the cost of battle is too dear and fever damages the very body it is defending. Autoimmune diseases provide another example of inflammation gone awry. The immune system targets the body’s own tissues by its inability to differentiate between some of the body’s proteins and foreign invaders. In essence, the immune system wages war, against itself. Diseases such as rheumatoid arthritis and lupus erythematosus are the result. Clearly, inflammation can be a double-edged sword.
News from the hot zone
Regarding Alzheimer’s disease, one research team noted, “Inflammation is becoming increasingly substantiated as a contributor to Alzheimer’s disease pathogenesis”1 For this reason anti-inflammatory drugs, such as the non-steroidal anti-inflammatory drugs (NSAIDs, e.g. aspirin, ibuprofen and acetaminophen) and the newer COX-2-inhibitor class of prescription drugs, are under investigation as therapies for this and other inflammation-related diseases.
Inflammation and the brain
Throughout most of the body, cells known as macrophages act as living soldiers, searching for invaders, and then engulfing and neutralizing them. In the brain, supporting cells of the glial family, known as microglial cells, act as scavengers, in much the same fashion as macrophages. They engulf and eliminate dead neurons that have been damaged by injury or illness. Unfortunately, they also secrete harmful neurotoxins and toxic oxygen free radicals in an attempt to neutralize foreign or undesirable substances.2
Regrettably, the inflammatory response is occasionally worse than the stimulus that triggered it in thefirst place. Even when the original trigger is eliminated, inflammation may become self-perpetuating. Such, apparently, is the case in neurodegenerative diseases such as Alzheimer’s, Parkinson’s, ALS and multiple sclerosis, which are characterized by a great deal of microglial activity. The presence of activated microglial cells is an indicator of chronic inflammation.3,4
Alzheimer’s and inflammation