Background: Few studies have examined structured rehabilitation techniques for improving activities of daily living in people with mild-moderate dementia. We sought to examine the advantages to delivering the Skill-building through Task-Oriented Motor Practice (STOMP) intervention in the home environment (versus the clinic), hypothesizing that ADL improvement would be significantly better, time to meeting goals would be faster and fewer displays of behavior would be noted.
Methods: Compared results of two quasi-experimental studies of STOMP, one completed in the home, one completed previously in a clinic. Participants were English-speaking; community dwelling adults aged 50-90 diagnosed with mild-moderate dementia who could participate in an intensive rehabilitation program (5 days/week, 3 hours/day, for 2 weeks). Outcome measurements include examiner-observation of performance and proxy-report of performance and satisfaction with performance in patient-selected goals.
Results: No differences existed in the sociodemographic characteristics between the home and clinic groups where the groups were primarily white, married, had > high school education and had mild-moderate dementia. Results from the home group indicate that participants made significant improvement in ADL which was generally retained at the 90 day follow-up. These results were not significantly different than the clinic group. No significant advantages were noted for the home group in terms of time to meeting goals or exhibition of fewer behaviors.
Discussion: The STOMP intervention appeared to work equally as well in the home and in the clinic. Future studies should continue to examine the benefits of massed practice using high-dose regimens.
Alzheimer's disease (AD) is the gradual loss of the cognitive function due to neuronal death. Currently no therapy is available to slow down, reverse or prevent the disease. Here we analyze the existing data in literature and hypothesize that the physiological function of the Amyloid Precursor Protein (APP) is activating the AppBp1 pathway and this function is gradually lost during the progression of AD pathogenesis. The AppBp1 pathway, also known as the neddylation pathway, activates the small ubiquitin-like protein nedd8, which covalently modifies and switches on Cullin ubiquitin ligases, which are essential in the turnover of cell cycle proteins. Here we discuss how APP may activate the AppBp1 pathway, which downregulates cell cycle markers and protects genome integrity. More investigation of this mechanism-driven hypothesis may provide insights into disease treatment and prevention strategies.
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