West Nile virus (WNV) is an RNA viral pathogen of the Flaviviridae family that is genetically related to CNS viral pathogens such as dengue, yellow fever, Japanese encephalitis and tick-borne encephalitis. The virus is maintained in the bird population and transmitted through a mosquito vector. When first described in 1940 (Smithburn et al. Am J Trop Med Hyg 1940;1:471-492) in a patient in Uganda, WNV infection produced a mild fever. But the virulence appeared to change in the 1990s with descriptions of severe WNV-associated neurological disease (Hubalek & Halouzka. Emerging Infect Dis 1999; 5:643-650).
Neurology
Apathy in Alzheimer’s disease a mortality risk factor
May 15, 2013Apathy in Alzheimer’s disease is characterized as diminished motivation lasting for at least four weeks, with reduced goal-directed behaviour, goal-directed cognitive activity and emotions, and accompanied by functional impairments (Robert et al. Eur Psychiatry 2009;24:98-104).
Effect of walking on cognitive function in Alzheimer’s disease
April 24, 2013A new study of early-stage Alzheimer’s disease reports that sedentary patients show significant deterioration in MMSE total score compared to more active patients, and that walking on a regular basis appears to stabilize cognitive decline (Winchester et al. Arch Gerontol Geriatr 2013;56:96-103). A total of 104 AD patients were followed over a 12-month period and categorized as Active or Sedentary based on Yale Physical Activity Survey scores.
Active patients who walked more than two hours per week had significant improvement in MMSE scores whereas Sedendary patients had significant worsening of MMSE scores.
Resistance training in PD: review of the evidence
April 24, 2013A systematic review of five controlled studies has concluded that resistance training can provide benefits to patients with Parkinson’s disease (Brienesse et al. J Am Med Dir Assoc 2013;14:236-241).
Uric acid and Parkinson’s disease
April 10, 2013Uric acid (UA) is the end product of purine metabolism in which adenosine, guanosine and inosine are broken down to form xanthine, which is converted to UA by xanthine oxidoreductase. In most mammals and other species, UA is further metabolized to allantoin by urate oxidase. In humans, a mutation to the UOx gene early in our evolution resulteprogred in an absence of functioning urate oxidase. In consequence, UA levels are as much as 10-fold higher in humans compared to other species (Alvarez-Lario & Macarron-Vicente. Rheumatology 2010;49:2010-2015).