A recent research article caught my eye, but more for this opening paragraph than the actual science:
Aging is the single greatest risk factor for Alzheimer's disease. In their latest study, researchers at the Salk Institute for Biological Studies found that simply slowing the aging process in mice prone to develop Alzheimer's disease prevented their brains from turning into a neuronal wasteland.
The emphasis is mine. Can you imagine such a thing being written ten years ago? Now it's old hat. We're just slowing the aging process in mice here, nothing to see, move along now. There are probably more than a dozen methods demonstrated to significantly slow down the effective rate of aging in mice, and more are being discovered with each passing year.
But on with the rest of the research. Diseases of aging, like Alzheimer's, might be considered as end-states of damage accumulation. It's the point at which slowly accumulated wear and tear reaches a threshold at which matters spiral down rapidly into system failure. Different types of damage lead to different diseases when they reach the runaway failure point, but the named conditions of aging can be thought of as the most common failure modes for worn human biology. Thus it makes sense that alterations shown to slow aging - in the sense of slowing damage accumulation - also protects against these conditions:
"In this study, we went directly to the root cause of Alzheimer's disease and asked whether we could influence the onset of the disease by modulating the aging process," says first author Ehud Cohen, Ph.D., formerly a postdoctoral researcher in Dillin's lab and now an assistant professor at the Hebrew University-Hadassah Medical School in Jerusalem, Israel.
To answer this intriguing question, he slowed the aging process in a mouse model for Alzheimer's by lowering the activity of the IGF-1 signaling pathway. "This highly conserved pathway plays a crucial role in the regulation of lifespan and youthfulness across many species, including worms, flies, and mice and is linked to extreme longevity in humans," he explains. As a result, mice with reduced IGF-1 signaling live up to 35 percent longer than normal mice.
Although long-lived mice didn't show any of the cognitive or behavioral impairments typical of Alzheimer's disease till very late in life, their brains were riddled with highly compacted plaques.
"Although before it was thought that plaques are the causative agents of Alzheimer's disease, our results clearly support the emerging theme that they have a protective function," says Cohen. "As mice age, they become less efficient at stowing away toxic beta amyloid fibrils in tightly packed aggregates."
As you might be aware, basic Alzheimer's research and theories of Alzheimer's biochemistry are in a very fluid state. The conclusions of past years are challenged on a regular basis, and a new consensus has yet to emerge. The data continues to flood in - it's an exciting field to be a part of these days, wherein anyone might soon establish the right connection that makes all the contradictions and datasets fall into place.