P7. Prevention and treatment of dementia
Detailed Programme, abstracts and presentations
P7. Prevention and treatment of dementia (Friday, 5 October, 16.00-17.30, Europa 1)
P7.1. Prevention of Alzheimer’s dementia: Strategies and current evidence
Primary prevention of Alzheimer‘s dementia is currently not feasible since the cause of the disease, with the exception of rare pathogenic mutations in the genes for the amyloid precursor and presenilin proteins, is still elusive. For secondary prevention three principal strategies can be envisaged: slowing the neurodegeneration, reducing cerebrovascular comorbidity, and strengthening brain reserve. Deceleration of the disease process has been attempted using antioxidants, non-steroidal anti-inflammatory drugs, lipid lowering agents, omega-3 polyunsaturated acids, and membrane protein precursors. Cerebrovas-cular comorbidity has been targeted using antihypertensive drugs, diabetes management, and treatment of dyslipidemia. Enhancement of brain reserve has been undertaken by means of cognitive or physical activity. Each one of these approaches is supported by evidence from observational studies showing that exposure to the potentially preventive factor is associated with a lower incidence of cognitive decline or dementia. However, since these investigations are uncontrolled, selection bias cannot be ruled out and causal conclusions cannot be drawn. With the aim of slowing the neurodegenerative process secretase inhibitors, anti-amyloid immunization, amyloid and tau aggregation blockers are under investigation. Randomized controlled trials have demonstrated that omega-3 polyunsaturated fatty acids and membrane protein precursors, gamma secretase inhibitors, anti-amyloid immunisation and amyloid aggregation blockers as well as cognitive and physical activity have favourable effects on cognitive ability. A weak effect on the incidence of cognitive decline or dementia has only been demonstrated for the long-term treatment of hypertension. More research is urgently needed to determine whether dietary, cognitive or physical interventions have preventive effects if applied over a sufficiently long time.
P7.2. Lifestyle Interventions to Protect against Dementia: Practical Recommendations based on Empirical Evidence
Michelle Kelly, Sabina Brennan
Thanks to improved healthcare, hygiene and nutrition, our life expectancy continues to rise. With increasing age however, comes an increase in the incidence of dementia. Most of us are aware of the prospective social and economic impact of the rising rates of dementia at European and global levels. While pharmacological interventions play an important role in managing dementia, a cure has not been forthcoming. Consequently, interest has grown in non-pharmacological interventions which may delay or even protect against dementia. A large body of research has been conducted, investigating the effects of lifestyle interventions such as leisure activity, exercise and diet on a variety of outcomes; with studies frequently citing encouraging results. Despite this, research in this area tends to be fragmented; with no standardization, little comparability across studies, and few empirical reviews capturing a number of interventions on a number of outcomes. In addition, many studies have made claims that have been sensationalized by popular press, leading to a misrepresentation of results in the public arena. This presentation will provide an overview of the research on lifestyle interventions (social and intellectual stimulation, exercise and diet), focusing on a number of outcomes including risk of dementia, cognitive performance, and neurological change. Practical recommendations will be made, aimed at informing the general public, and based on sufficient empirical evidence. The work presented is the outcome of a joint initiative between the NEIL Program at Trinity College Dublin and the Alzheimer’s Society of Ireland who have come together “to promote healthy ageing by transforming empirical data into useable, interpretable and practical health and well-being information”.
P7.3. Antipsychotic prescribing for dementia in a care home setting
Background: Despite warnings about increased mortality in dementia patients treated with antipsychotics1, studies report that up to 30% of care-home residents with dementia are still treated with antipsychotic drugs2. It is suggested that some doctors feel pressured to prescribe due to lack of resources and viable alternative treatments3. This study will assess if lower levels of antipsychotic prescribing for dementia are achievable in a care-home setting which has implemented a policy of, where possible, reducing antipsychotic prescribing in dementia, in favour of non-pharmacological intervention.
Method: Search of computer and paper records for residents prescribed antipsychotic drugs for dementia.
Results: Of 99 residents with a diagnosed dementia, 9% were being treated with antipsychotic drugs.
Conclusions: These prescribing levels are significantly lower than those found in previous studies. Evidently, with appropriate direction it is possible to avoid high levels of antipsychotic prescribing for dementia in care home settings. Further study is required to assess levels of antipsychotic prescribing in a larger population.
P7.4. The effect of the medical food Souvenaid on memory performance and synaptic activity in patients with mild Alzheimer’s Disease
Philip Scheltens, Jos Twisk, PRafael Blesa, Elio Scarpini, Christine von Arnim, Anke Bongers, John Harrison, Sophie Swinkels, Cornelis Stam, Hanneke de Waal, Richard Wurtman, Rico Wieggers, Bruno Vellas, Patrick Kamphuis
Background: Souvenaid, containing the specific nutrient combination Fortasyn Connect, is designed to support synapse formation and function in Alzheimer’s disease (AD). Synaptic dysfunction is a pathological process already involved in the early stages of AD, which causes disruption in neuronal connectivity and correlates strongly with cognitive dysfunction. In a proof-of-concept study with drug-naïve patients with mild AD (MMSE 20-26), 12-week intervention with Souvenaid improved memory performance. The Souvenir II study was designed to confirm and extend these findings to a 24-week intervention period.
Method: The Souvenir II study (NTR1975)1 was a 24-week randomised controlled double- blind study in 259 drug-naïve mild AD patients (MMSE ≥ 20). Patients received either Souvenaid or isocaloric control product. Primary outcome measure was the memory domain score resulting from a neuropsychological test battery (NTB). Secondary outcomes included the NTB executive function domain score, the NTB, total score, the Disability Assessment for Dementia (DAD) scale, safety, tolerance and compliance. Electroencephalography (EEG) measures were included as secondary outcomes as a marker for synaptic activity and connectivity. Functional brain connectivity was investigated using the phase lag index (PLI). Groups were compared using mixed model for repeated measures.
Results: The Souvenir II study showed that Souvenaid significantly increased the NTB memory domain score over 24 weeks in patients with mild AD, compared to the control product. No effect was found on the DAD and on the NTB executive function domain. A trend was observed for the effect on the NTB total score. EEG analyses yielded a significant difference between study groups for functional connectivity (PLI) over 24 weeks in favour of the Souvenaid group. Souvenaid was well-tolerated, with a high compliance (97%).
Conclusion: The present study supports and extends the earlier findings that Souvenaid improves memory performance in patients with mild AD. Similar to previous observations, this 24-week study showed that Souvenaid was well-tolerated. The EEG results suggest that Souvenaid enhances neuronal connectivity in mild AD, possibly by improving synapse function.
Last Updated: jeudi 15 novembre 2012