Long life still hard on the brain

The average life expectancy in the US has hit a record high of 77.6 years. The Centers for Disease Control attribute this statistic to declining death rates from heart disease, cancer, stroke, HIV/AIDS, drug abuse, and firearms. But as the aging population increases, so does the risk for age-related syndromes such as Parkinson disease (PD) and Alzheimer disease (AD), for which there are no cures. Recent research offers a better understanding of the etiology of these neurodegenerative diseases and hope for future treatment. In the February 25, 2005, issue of Science, researchers discovered axonal defects that precede known AD pathology — swellings along axons containing cellular motor proteins, organelles, and vesicles (1). Hindering the axonal motor transport machinery amplified the frequency of these defects and increased amyloid deposits in the brains of mice with AD. These findings indicate that decreased axonal transport might promote the formation of senile plaques characteristic of AD. Another study, published in the April issue of the American Journal of Human Genetics, shows that a novel mutation in the leucine-rich repeat kinase 2 (LRRK2) gene causes a genetic component of PD in several families (2). These new insights into the pathophysiology of age-related neurodegenerative diseases will help ease the burden on the growing elderly population.

References

1. Stokin, GB, et al. RAxonopathy and transport deficits early in the pathogenesis of Alzheimer’s disease. Science 2005. 307:1282-1288.
   View this article via: PubMed CrossRef Google Scholar
2. Kachergus, J, et al. Identification of a novel LRRK2 mutation linked to autosomal dominant parkinsonism: evidence of a common founder across European populations. Am. J. Hum. Genet. 2005. 76:672-680.
   View this article via: PubMed CrossRef Google Scholar