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Web-based CBT effective for depression, QOL

May 8, 2013

The Australian National University, Canberra, reports that a web-based cognitive-behavioural therapy (CBT) program can be an effective tool in improving depression and quality of life. Callers to a national helpline with moderate to high psychological distress were randomized to an Internet CBT program, weekly telephone follow-ups, Internet CBT plus weekly telephone follow-up, or usual care (Farrer et al. PLoS One 2011;6:e28099; free full text at www.ncbi.nlm.nih.gov/pmc/articles/PMC3227639/pdf/pone.0028099.pdf).

Mean patient age was 37-43 years, 82% of participants were female and 53% were not employed. Most (93%) had a history of depression, 60% had a history of social phobia, and 74% had experienced a panic attack in the preceding four weeks.

Effect of walking on cognitive function in Alzheimer’s disease

April 24, 2013

A 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, 2013

A 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, 2013

Uric 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).

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