McKee K.E., Hackney M.E. for both AD and PD. Furthermore, in light of the diverse constellation of other neuropsychiatric, physical, and behavioural symptoms that often occur in AD and PD, consideration needs to be given to the potential side effects of pharmacological treatments where improving one symptom may lead to the worsening of another, rendering the clinical management of these patients challenging. Therefore, the present article will critically review the evidence for both pharmacological and non-pharmacological treatments for cognitive impairment in AD and PD patients. Treatment options for other concomitant neuropsychiatric and behavioural symptoms, as well as novel treatment strategies will also be discussed. = 195), or 10mg Donepezil (= 182), or placebo (= 173) for Anitrazafen 24 weeks. No significant difference was observed between the treatment groups and the placebo group on the primary outcome measures of ADAS-Cog and the CIBIC-plus, although results on the CIBIC-plus and the ADAS-Cog for the 10mg group (but not the 5mg group), showed statistically Anitrazafen significant superiority compared to the placebo group in relation to primary outcome measures. Significant differences on some secondary measures including the MMSE, and some cognitive measures (and studies have suggested that Memantine may also have neuroprotective potential. However, more data to confirm such activity is required [69]. The benefits of Memantine have been explored in a few RCTs evaluating patients with PDD. However, results regarding its efficacy have been conflicting [78, 79]. In one study in which Aarsland = 42) more so than those treated with placebo. It was reported that probable RBD, as assessed by the Stavanger Sleep Questionnaire, was decreased by Memantine, and both diagnostic groups (PDD and DLB) contributed equally to the outcome. However, no significant improvement was observed in the severity of excessive daytime sleepiness. Memantine also appeared to be well tolerated in both diagnostic groups. At present, there are no approved treatments for sleep disturbances in PD. Nevertheless, several drug agents may hold some promise in treating sleep disturbances in PD. This includes Modafanil for the treatment of excessive daytime sleepiness, Eszopiclone for insomnia, as well as Clonazepam and Melatonin for RBD (for a review, see Trotti and Bliwise (2014) [155]). However, the potential side effects of Clonazepam, such as excessive daytime sleepiness, confusion, and cognitive impairment, may limit Anitrazafen its usefulness in the PD population [155]. Such findings are encouraging and suggest the need for exploration in PDD patients. 6.?CONCLUSION In conclusion, research on pharmacological therapies for AD and PDD has so far had some success in terms of developing symptomatic treatments (See Table ?11. for summary). However, research is needed to develop a broader and more fundamental therapeutic approach to both AD and PD, including an emphasis on disease-modifying therapies. Until new preventive or disease-modifying treatments are approved, it is vital that clinicians optimize the use of available pharmacological and non-pharmacological interventions for AD and PDD. For patients with mild to moderate AD, ChEIs are the traditional first line of pharmacological treatment, whereas for patients with moderate to severe AD, treatment with Memantine and Donepezil Anitrazafen are both indicated. With regard to patients with mild to moderate PDD, Rivastigmine is currently the only approved pharmacological treatment. In addition, non-pharmacological therapies, such as cognitive training and exercise may also play a role in improving cognitive functioning in these populations. However, well designed studies are needed to provide more definitive evidence. The treatment of any co-existing conditions in both AD and PDD patients is also vital as they may aggravate pre-existing cognitive deficits. Importantly, treatments for such symptoms require careful consideration as they may not be part of the disease process itself, and may result from other factors, such as side effects related to the treatment administered. Furthermore, the drug interactions between medications for PD (positron emission tomographic study. Arch. Neurol. 2003;60(12):1745C1748. doi:?10.1001/archneur.60.12.1745. [PubMed] [CrossRef] [Google Scholar] 18. Perry E.K., Irving D., Kerwin J.M., McKeith I.G., Thompson P., Collerton D., Fairbairn A.F., Ince P.G., Morris C.M., Cheng A.V., Perry R.H. 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