Podcast
Questions and Answers
What is the most common form of dementia?
What is the most common form of dementia?
What are Neuropsychiatric symptoms (NPSs)?
What are Neuropsychiatric symptoms (NPSs)?
What are the consequences of Neuropsychiatric symptoms (NPSs) in patients with dementia?
What are the consequences of Neuropsychiatric symptoms (NPSs) in patients with dementia?
What do clinical treatment guidelines recommend for the treatment of Neuropsychiatric symptoms (NPSs) in dementia?
What do clinical treatment guidelines recommend for the treatment of Neuropsychiatric symptoms (NPSs) in dementia?
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What is the treatment algorithm for Neuropsychiatric symptoms (NPSs) in patients with dementia?
What is the treatment algorithm for Neuropsychiatric symptoms (NPSs) in patients with dementia?
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What is the effectiveness of atypical antipsychotics (AAPs) in improving psychosis or agitation in patients with Alzheimer's disease according to the Clinical Antipsychotic Trials of Intervention Effectiveness-Alzheimer's Disease (CATIE-AD) trial?
What is the effectiveness of atypical antipsychotics (AAPs) in improving psychosis or agitation in patients with Alzheimer's disease according to the Clinical Antipsychotic Trials of Intervention Effectiveness-Alzheimer's Disease (CATIE-AD) trial?
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What are the consequences of treatment-resistant Neuropsychiatric symptoms (NPSs) in patients with dementia?
What are the consequences of treatment-resistant Neuropsychiatric symptoms (NPSs) in patients with dementia?
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What are non-pharmacological interventions for the treatment of Neuropsychiatric symptoms (NPSs) in patients with dementia?
What are non-pharmacological interventions for the treatment of Neuropsychiatric symptoms (NPSs) in patients with dementia?
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What is the importance of elucidating the pathogeneses of treatment-resistant Neuropsychiatric symptoms (NPSs) in patients with dementia?
What is the importance of elucidating the pathogeneses of treatment-resistant Neuropsychiatric symptoms (NPSs) in patients with dementia?
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What model should be discussed to resolve the unknown mechanisms underlying treatment-resistant Neuropsychiatric symptoms (NPSs) in patients with dementia?
What model should be discussed to resolve the unknown mechanisms underlying treatment-resistant Neuropsychiatric symptoms (NPSs) in patients with dementia?
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What is the first-choice medicine for treating the crucial sub-symptoms of Neuropsychiatric symptoms (NPSs) in patients with dementia?
What is the first-choice medicine for treating the crucial sub-symptoms of Neuropsychiatric symptoms (NPSs) in patients with dementia?
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What is the most common form of dementia?
What is the most common form of dementia?
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What are Neuropsychiatric symptoms (NPSs)?
What are Neuropsychiatric symptoms (NPSs)?
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What do clinical treatment guidelines recommend for the treatment of Neuropsychiatric symptoms (NPSs) in dementia?
What do clinical treatment guidelines recommend for the treatment of Neuropsychiatric symptoms (NPSs) in dementia?
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What is the treatment algorithm for Neuropsychiatric symptoms (NPSs) in patients with dementia?
What is the treatment algorithm for Neuropsychiatric symptoms (NPSs) in patients with dementia?
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What model should be discussed to resolve the unknown mechanisms underlying treatment-resistant Neuropsychiatric symptoms (NPSs) in patients with dementia?
What model should be discussed to resolve the unknown mechanisms underlying treatment-resistant Neuropsychiatric symptoms (NPSs) in patients with dementia?
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What are neuropsychiatric symptoms (NPSs)?
What are neuropsychiatric symptoms (NPSs)?
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What is the impact of NPSs on patients with dementia?
What is the impact of NPSs on patients with dementia?
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What is the treatment algorithm for NPSs in patients with dementia?
What is the treatment algorithm for NPSs in patients with dementia?
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What is the effectiveness of atypical antipsychotics (AAPs) for improving psychosis or agitation in patients with Alzheimer's disease?
What is the effectiveness of atypical antipsychotics (AAPs) for improving psychosis or agitation in patients with Alzheimer's disease?
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Why do patients discontinue treatment during phase 1 of the CATIE-AD trial?
Why do patients discontinue treatment during phase 1 of the CATIE-AD trial?
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Are non-pharmacological interventions for the treatment of NPSs effective?
Are non-pharmacological interventions for the treatment of NPSs effective?
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What is the importance of elucidating the pathogeneses of NPSs that are difficult to treat pharmacologically?
What is the importance of elucidating the pathogeneses of NPSs that are difficult to treat pharmacologically?
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What model should be discussed to resolve the unknown mechanisms underlying treatment-resistant NPSs?
What model should be discussed to resolve the unknown mechanisms underlying treatment-resistant NPSs?
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What is the definition of treatment-resistant schizophrenia (TRS)?
What is the definition of treatment-resistant schizophrenia (TRS)?
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What is the definition of treatment-resistant depression (TRD)?
What is the definition of treatment-resistant depression (TRD)?
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What is pharmacological treatment-resistant NPSs in AD (p-TRENS-AD)?
What is pharmacological treatment-resistant NPSs in AD (p-TRENS-AD)?
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Which of the following NPSs in AD are unlikely to respond to pharmacological treatment?
Which of the following NPSs in AD are unlikely to respond to pharmacological treatment?
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What are some factors that can contribute to the development of p-TRENS-AD?
What are some factors that can contribute to the development of p-TRENS-AD?
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What is necessary for the prescription of antipsychotics?
What is necessary for the prescription of antipsychotics?
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Do older patients with schizophrenia have a higher or lower therapeutic window than younger patients?
Do older patients with schizophrenia have a higher or lower therapeutic window than younger patients?
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How can changes in the central drug absorption system in the AD-affected brain affect antipsychotics?
How can changes in the central drug absorption system in the AD-affected brain affect antipsychotics?
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How can cytochrome P450 isoforms affect drug treatment in AD patients?
How can cytochrome P450 isoforms affect drug treatment in AD patients?
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Can pharmacogenomics predict treatment response in AD patients with depression?
Can pharmacogenomics predict treatment response in AD patients with depression?
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What are the theoretical neuropharmacological mechanisms of NPSs in AD?
What are the theoretical neuropharmacological mechanisms of NPSs in AD?
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Can pharmacological treatment with antipsychotics accelerate apathy or motivation loss in AD patients?
Can pharmacological treatment with antipsychotics accelerate apathy or motivation loss in AD patients?
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What is the definition of p-TRENS-AD?
What is the definition of p-TRENS-AD?
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What is the definition of TRS?
What is the definition of TRS?
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What is the definition of TRD?
What is the definition of TRD?
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Which NPSs in AD are unlikely to respond to pharmacological treatment?
Which NPSs in AD are unlikely to respond to pharmacological treatment?
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What factors can contribute to the development of p-TRENS-AD?
What factors can contribute to the development of p-TRENS-AD?
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What is the role of age-related alterations in pharmacokinetics in p-TRENS-AD?
What is the role of age-related alterations in pharmacokinetics in p-TRENS-AD?
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What is the optimal occupancy of striatal dopamine D2/3 receptors necessary for the prescription of antipsychotics?
What is the optimal occupancy of striatal dopamine D2/3 receptors necessary for the prescription of antipsychotics?
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What changes in the central drug absorption system in the AD-affected brain may increase the affinity of antipsychotics to the D2/3 receptor?
What changes in the central drug absorption system in the AD-affected brain may increase the affinity of antipsychotics to the D2/3 receptor?
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What may exacerbate undesirable effects via drug-drug interactions?
What may exacerbate undesirable effects via drug-drug interactions?
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What can pharmacogenomics predict in patients with major depressive disorder (MDD)?
What can pharmacogenomics predict in patients with major depressive disorder (MDD)?
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What are the theoretical neuropharmacological mechanisms of NPSs in AD?
What are the theoretical neuropharmacological mechanisms of NPSs in AD?
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What is the potential drawback of pharmacological treatment with antipsychotics for monoaminergic hyper-availability state leading to delusion and aggressiveness?
What is the potential drawback of pharmacological treatment with antipsychotics for monoaminergic hyper-availability state leading to delusion and aggressiveness?
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What is pharmacological treatment-resistant NPSs in AD (p-TRENS-AD)?
What is pharmacological treatment-resistant NPSs in AD (p-TRENS-AD)?
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What is the definition of treatment-resistant schizophrenia (TRS)?
What is the definition of treatment-resistant schizophrenia (TRS)?
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What is the definition of treatment-resistant depression (TRD)?
What is the definition of treatment-resistant depression (TRD)?
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What are some sub-symptoms in AD that are unlikely to respond to pharmacological treatment?
What are some sub-symptoms in AD that are unlikely to respond to pharmacological treatment?
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What factors can contribute to the development of p-TRENS-AD?
What factors can contribute to the development of p-TRENS-AD?
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How can age-related alterations in pharmacokinetics affect drug clearance?
How can age-related alterations in pharmacokinetics affect drug clearance?
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What is necessary for the prescription of antipsychotics?
What is necessary for the prescription of antipsychotics?
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What changes in the central drug absorption system in the AD-affected brain may lead to increased permeability across the blood-brain barrier?
What changes in the central drug absorption system in the AD-affected brain may lead to increased permeability across the blood-brain barrier?
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How can Cytochrome P450 isoforms affect drug-drug interactions?
How can Cytochrome P450 isoforms affect drug-drug interactions?
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What can pharmacogenomics predict in patients with major depressive disorder (MDD)?
What can pharmacogenomics predict in patients with major depressive disorder (MDD)?
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What are the theoretical neuropharmacological mechanisms of NPSs in AD?
What are the theoretical neuropharmacological mechanisms of NPSs in AD?
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What is the potential effect of pharmacological treatment with antipsychotics on monoaminergic hyper-availability state leading to delusion and aggressiveness?
What is the potential effect of pharmacological treatment with antipsychotics on monoaminergic hyper-availability state leading to delusion and aggressiveness?
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What is the reason for treatment discontinuation in Alzheimer's disease?
What is the reason for treatment discontinuation in Alzheimer's disease?
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What approach is needed to reduce the risk of adverse effects in elderly people with Alzheimer's disease?
What approach is needed to reduce the risk of adverse effects in elderly people with Alzheimer's disease?
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What contributes to adverse effects in elderly patients with Alzheimer's disease?
What contributes to adverse effects in elderly patients with Alzheimer's disease?
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What may increase the affinity of antipsychotics to the D2/3 receptor in Alzheimer's disease-affected brains?
What may increase the affinity of antipsychotics to the D2/3 receptor in Alzheimer's disease-affected brains?
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What exacerbates adverse effects via drug-drug interactions in patients with Alzheimer's disease?
What exacerbates adverse effects via drug-drug interactions in patients with Alzheimer's disease?
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What gene polymorphisms significantly predict antidepressant response in patients with major depressive disorder?
What gene polymorphisms significantly predict antidepressant response in patients with major depressive disorder?
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What has a better response to treatment for depression and anxiety in patients with Alzheimer's disease been associated with?
What has a better response to treatment for depression and anxiety in patients with Alzheimer's disease been associated with?
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Which metabolic genophenotypes of the CYP enzymes respond significantly better to current treatments for depression and anxiety in patients with Alzheimer's disease?
Which metabolic genophenotypes of the CYP enzymes respond significantly better to current treatments for depression and anxiety in patients with Alzheimer's disease?
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What is the difference between the theoretical neuropharmacological mechanism of psychosis in Alzheimer's disease and schizophrenia?
What is the difference between the theoretical neuropharmacological mechanism of psychosis in Alzheimer's disease and schizophrenia?
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What factors have been associated with the emergence of neuropsychiatric symptoms (NPS) in Alzheimer's disease?
What factors have been associated with the emergence of neuropsychiatric symptoms (NPS) in Alzheimer's disease?
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What may influence the occurrence of NPSs in Alzheimer's disease, causing interpersonal problems between patients and caregivers via psychopathological conflicts?
What may influence the occurrence of NPSs in Alzheimer's disease, causing interpersonal problems between patients and caregivers via psychopathological conflicts?
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What can contribute indirectly to a reduction in the severity of NPS in patients with dementia?
What can contribute indirectly to a reduction in the severity of NPS in patients with dementia?
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What is the reason for treatment discontinuation in Alzheimer's disease?
What is the reason for treatment discontinuation in Alzheimer's disease?
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Why is a 'start low, go slow' approach needed for pharmacological treatments in elderly patients with Alzheimer's disease?
Why is a 'start low, go slow' approach needed for pharmacological treatments in elderly patients with Alzheimer's disease?
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What contributes to adverse effects in elderly patients with Alzheimer's disease?
What contributes to adverse effects in elderly patients with Alzheimer's disease?
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What changes occur in the central drug absorption system in the AD-affected brain?
What changes occur in the central drug absorption system in the AD-affected brain?
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What exacerbates adverse effects in patients with AD?
What exacerbates adverse effects in patients with AD?
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What predicts antidepressant response in patients with major depressive disorder?
What predicts antidepressant response in patients with major depressive disorder?
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What is associated with a better response to treatment for depression and anxiety in patients with AD?
What is associated with a better response to treatment for depression and anxiety in patients with AD?
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Which metabolic genophenotypes respond significantly better to current treatments for depression and anxiety in patients with AD?
Which metabolic genophenotypes respond significantly better to current treatments for depression and anxiety in patients with AD?
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What is the difference between the theoretical neuropharmacological mechanism of psychosis in AD and schizophrenia?
What is the difference between the theoretical neuropharmacological mechanism of psychosis in AD and schizophrenia?
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What factors have been associated with the emergence of neuropsychiatric symptoms (NPS) in AD?
What factors have been associated with the emergence of neuropsychiatric symptoms (NPS) in AD?
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How do psychosocial and demographic factors influence the occurrence of NPS in AD?
How do psychosocial and demographic factors influence the occurrence of NPS in AD?
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How can comprehensive non-pharmacological interventions for cohabitant caregivers contribute to a reduction in the severity of NPS in patients with dementia?
How can comprehensive non-pharmacological interventions for cohabitant caregivers contribute to a reduction in the severity of NPS in patients with dementia?
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What is the reason for treatment discontinuation in Alzheimer's disease?
What is the reason for treatment discontinuation in Alzheimer's disease?
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What approach is needed to reduce the risk of adverse effects in elderly patients with AD?
What approach is needed to reduce the risk of adverse effects in elderly patients with AD?
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How do age-related alterations in peripheral pharmacokinetics affect drug clearance?
How do age-related alterations in peripheral pharmacokinetics affect drug clearance?
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What changes in the central drug absorption system may increase the affinity of antipsychotics to the D2/3 receptor in the AD-affected brain?
What changes in the central drug absorption system may increase the affinity of antipsychotics to the D2/3 receptor in the AD-affected brain?
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What contributes to adverse effects via drug-drug interactions arising from the concomitant use of multiple medicines prescribed for lifestyle-related diseases in elderly patients with AD?
What contributes to adverse effects via drug-drug interactions arising from the concomitant use of multiple medicines prescribed for lifestyle-related diseases in elderly patients with AD?
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What has been associated with a better response to treatment for depression and anxiety in patients with AD?
What has been associated with a better response to treatment for depression and anxiety in patients with AD?
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What are the metabolic genophenotypes of the CYP enzymes?
What are the metabolic genophenotypes of the CYP enzymes?
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Which patients with AD responded significantly better to current treatments for depression and anxiety?
Which patients with AD responded significantly better to current treatments for depression and anxiety?
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What is the theoretical neuropharmacological mechanism of psychosis in AD?
What is the theoretical neuropharmacological mechanism of psychosis in AD?
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What factors have been associated with NPS emergence in AD?
What factors have been associated with NPS emergence in AD?
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What may influence the occurrence of NPSs in AD, causing interpersonal problems between patients and caregivers via psychopathological conflicts?
What may influence the occurrence of NPSs in AD, causing interpersonal problems between patients and caregivers via psychopathological conflicts?
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What can contribute indirectly to a reduction in the severity of NPS in patients with dementia?
What can contribute indirectly to a reduction in the severity of NPS in patients with dementia?
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What are some factors that may hinder treatment response to pharmacological interventions for neuropsychiatric symptoms in Alzheimer's disease?
What are some factors that may hinder treatment response to pharmacological interventions for neuropsychiatric symptoms in Alzheimer's disease?
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What are some NPS sub-symptoms that can be caused by neurocognitive mechanisms in AD?
What are some NPS sub-symptoms that can be caused by neurocognitive mechanisms in AD?
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What is a potential consequence of poor self-awareness of cognitive symptoms and NPS in AD?
What is a potential consequence of poor self-awareness of cognitive symptoms and NPS in AD?
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What are some first-line approaches for reducing NPS severity in dementia?
What are some first-line approaches for reducing NPS severity in dementia?
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What is a potential benefit of relocating AD patients into specialized care units?
What is a potential benefit of relocating AD patients into specialized care units?
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What is a potential alternative treatment for AD patients with apathy or depression?
What is a potential alternative treatment for AD patients with apathy or depression?
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What is the placebo effect on NPS in AD patients?
What is the placebo effect on NPS in AD patients?
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What are some potential side effects and risks of medications when treating NPS in AD patients?
What are some potential side effects and risks of medications when treating NPS in AD patients?
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What is the potential benefit of reducing NPS in AD patients?
What is the potential benefit of reducing NPS in AD patients?
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What are some non-pharmacological interventions that can be effective in reducing NPS?
What are some non-pharmacological interventions that can be effective in reducing NPS?
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What is a potential drawback of continuation of antipsychotic drugs for treatment of psychosis or agitation in AD patients?
What is a potential drawback of continuation of antipsychotic drugs for treatment of psychosis or agitation in AD patients?
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What is the potential benefit of long-term treatment strategies based on neurocognitive mechanisms for p-TRENS-AD?
What is the potential benefit of long-term treatment strategies based on neurocognitive mechanisms for p-TRENS-AD?
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What is the first-line approach for reducing NPS severity in dementia?
What is the first-line approach for reducing NPS severity in dementia?
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What is the placebo effect on NPS in AD patients?
What is the placebo effect on NPS in AD patients?
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What are the main NPS in Alzheimer's disease?
What are the main NPS in Alzheimer's disease?
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What can cause pessimistic ideation and suicidal behavior in AD patients?
What can cause pessimistic ideation and suicidal behavior in AD patients?
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What is the CATIE-AD trial?
What is the CATIE-AD trial?
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What is the recommended treatment for hallucinations and delusions in AD patients?
What is the recommended treatment for hallucinations and delusions in AD patients?
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What can hinder treatment response to pharmacological interventions for NPS in AD?
What can hinder treatment response to pharmacological interventions for NPS in AD?
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What percentage of reduction in NPS severity was observed in the placebo group of the CATIE-AD trial?
What percentage of reduction in NPS severity was observed in the placebo group of the CATIE-AD trial?
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What can patient relocation into specialized care units improve in AD patients?
What can patient relocation into specialized care units improve in AD patients?
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What are the potential risks of medications when treating NPS in AD patients?
What are the potential risks of medications when treating NPS in AD patients?
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What is the recommended treatment for depression and anxiety in AD patients?
What is the recommended treatment for depression and anxiety in AD patients?
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What can hinder targeted treatment for complex NPS sub-symptoms in AD patients?
What can hinder targeted treatment for complex NPS sub-symptoms in AD patients?
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What are some factors that may hinder treatment response to pharmacological interventions for neuropsychiatric symptoms in AD?
What are some factors that may hinder treatment response to pharmacological interventions for neuropsychiatric symptoms in AD?
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What are some neuropsychiatric symptoms (NPS) commonly seen in AD patients?
What are some neuropsychiatric symptoms (NPS) commonly seen in AD patients?
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What are some non-pharmacological interventions that can be effective in reducing NPS in AD patients?
What are some non-pharmacological interventions that can be effective in reducing NPS in AD patients?
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What is the placebo effect on NPS in AD patients?
What is the placebo effect on NPS in AD patients?
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What are some potential risks of medications when treating NPS in AD patients?
What are some potential risks of medications when treating NPS in AD patients?
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What are some first-line approaches for reducing NPS severity in dementia?
What are some first-line approaches for reducing NPS severity in dementia?
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What is CATIE-AD trial and what was its main finding?
What is CATIE-AD trial and what was its main finding?
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What are some factors that can influence the presence of loneliness and other life changes in AD patients?
What are some factors that can influence the presence of loneliness and other life changes in AD patients?
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What are some treatments for bipolar symptoms in AD patients?
What are some treatments for bipolar symptoms in AD patients?
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What is p-TRENS-AD and what is the recommended treatment strategy for it?
What is p-TRENS-AD and what is the recommended treatment strategy for it?
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What are some alternative treatments for AD patients with apathy or depression?
What are some alternative treatments for AD patients with apathy or depression?
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What is the potential benefit of reducing NPS in AD patients?
What is the potential benefit of reducing NPS in AD patients?
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Study Notes
Challenges in Pharmacological Treatment for Neuropsychiatric Symptoms in Patients with Dementia
- The prevalence of patients with dementia worldwide is expected to reach about 152 million by 2050.
- Alzheimer's disease is the most common form of dementia and is characterized by progressive neurocognitive impairments, leading to reductions in daily activities.
- Neuropsychiatric symptoms (NPSs) such as psychosis, agitation, depression, and apathy appear during the course of dementia.
- NPSs worsen patients' prognoses, resulting in a shorter life span, earlier institutionalization, more severe caregiver burden, and increased socio-economic burden.
- Clinical treatment guidelines for NPSs in dementia recommend non-pharmacological interventions rather than pharmacological interventions.
- The treatment algorithm for NPSs in patients with dementia requires definitive, urgent conditions for pharmacological treatment.
- Antipsychotics have conventionally been presumed to be more effective than other medicines for improving psychosis or agitation in patients with AD.
- The Clinical Antipsychotic Trials of Intervention Effectiveness-Alzheimer's Disease (CATIE-AD) trial could not show significant effectiveness of atypical antipsychotics (AAPs) compared with a placebo, and about 80% of patients discontinued treatment during phase 1 due to undesirable adverse effects or lack of efficacy.
- The crucial sub-symptoms (psychosis, agitation, and depression) of NPSs that necessitate urgent pharmacological interventions tend to be difficult to treat, with the first-choice medicine often having to be switched to another drug.
- Non-pharmacological interventions for the treatment of NPSs may be relatively weak alternatives to pharmacological treatments.
- Elucidating the pathogeneses of NPSs that are difficult to treat pharmacologically may be helpful to clinicians and caregivers during discussions regarding long-term care plans and treatment strategies.
- A bio-psychosocial-neurocognitive model should be discussed to resolve the unknown mechanisms underlying treatment-resistant NPSs, including delusional misidentification and apathy.
Pharmacological Treatment-Resistant Neuropsychiatric Symptoms in Alzheimer's Disease: Definition and Hypothetical Pathogenesis
- Pharmacological treatment difficulties have been defined in patients with mental disorders, but not in those with neuropsychiatric symptoms (NPSs) in Alzheimer's disease (AD).
- Treatment-resistant schizophrenia (TRS) is defined as poor response despite adequate treatment, while treatment-resistant depression (TRD) is defined as failure to achieve treatment response after at least two adequate trials of antidepressants.
- Pharmacological treatment-resistant NPSs in AD (p-TRENS-AD) refers to urgent sub-symptoms that are likely to respond poorly to pharmacological treatment or for which pharmacological treatment is likely to be intolerable.
- Sub-symptoms such as wandering, perseverative shouting, and some sexually inappropriate behaviors are unlikely to respond to pharmacological treatment.
- Biological and psychosocial factors can contribute to the development of p-TRENS-AD.
- Age-related alterations in pharmacokinetics can reduce drug clearance and contribute to adverse effects.
- An optimal occupancy of striatal dopamine D2/3 receptors is necessary for the prescription of antipsychotics, but older patients with schizophrenia may have a lower therapeutic window than younger patients.
- Changes in the central drug absorption system in the AD-affected brain may increase the affinity of antipsychotics to the D2/3 receptor, leading to increased permeability across the blood-brain barrier.
- Cytochrome P450 isoforms may exacerbate undesirable effects via drug-drug interactions.
- Pharmacogenomics can predict treatment response in patients with major depressive disorder (MDD), but other factors may influence the subsequent prognosis in AD patients with depression.
- Theoretical neuropharmacological mechanisms of NPSs in AD involve the involvement of monoaminergic neurons, including the serotonergic dorsal raphe nucleus and the noradrenergic locus coeruleus.
- Pharmacological treatment with antipsychotics may be effective against monoaminergic hyper-availability state leading to delusion and aggressiveness, but may tend to accelerate apathy or motivation loss.
Factors Influencing Treatment Response in Elderly Patients with Alzheimer's Disease
- Treatment discontinuation in Alzheimer's disease (AD) is due to adverse effects and lack of efficacy, leading to the need for alternative medications.
- Elderly people may have difficulty tolerating pharmacological treatments, and a "start low, go slow" approach is needed to reduce the risk of adverse effects.
- Age-related alterations in peripheral pharmacokinetics reduce drug clearance, contributing to adverse effects.
- Within the AD-affected brain, changes in the central drug absorption system arising from the disruption of the blood-brain barrier may increase the affinity of antipsychotics to the D2/3 receptor.
- Cytochrome P450 isoforms may exacerbate adverse effects via drug-drug interactions arising from the concomitant use of multiple medicines prescribed for lifestyle-related diseases.
- Antidepressant response in patients with major depressive disorder is significantly predicted by candidate gene polymorphisms, but not associated with CYP genes.
- A better response to treatment for depression and anxiety in patients with AD has been associated with APOE-ε3 carriers.
- The metabolic genophenotypes of the CYP enzymes can be classified as normal metabolizer, intermediate metabolizer, poor metabolizer, or ultra-rapid metabolizer, and patients with AD who were classified as NMs or IMs responded significantly better to current treatments for depression and anxiety than those who were classified as PMs or UMs.
- The theoretical neuropharmacological mechanism of psychosis in AD is subtly different from that for schizophrenia mainly because of the relevance of the monoaminergic neurocircuitry.
- Severe caregiver burden, housemate type, racial type, educational level, sex, marital status, residential situation, and comorbidities other than NPS sub-symptoms have been associated with NPS emergence.
- The reciprocal relationship between psychosocial factors and demographic ones may influence the occurrence of NPSs in AD, causing interpersonal problems between patients and caregivers via psychopathological conflicts.
- Comprehensive non-pharmacological interventions for cohabitant caregivers can contribute indirectly to a reduction in the severity of NPS in patients with dementia.
Strategies for Treating Treatment-Resistant Neuropsychiatric Symptoms in Alzheimer's Disease
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Neglecting psychosocial and demographic factors may hinder treatment response to pharmacological interventions for neuropsychiatric symptoms (NPS) in Alzheimer's disease (AD).
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Gender differences in AD patients can influence the presence of cohabitant and marital status, which may be associated with loneliness and other life changes.
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Neurocognitive mechanisms in AD can cause complex NPS sub-symptoms, including apathy, disinhibition, and depression, hindering targeted treatment.
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The severity and frequency of cognitive decline in AD patients can influence NPS sub-symptoms and treatment response.
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Poor self-awareness of cognitive symptoms and NPS in AD can lead to refusal of care and delay treatment intervention, while preserved self-awareness can cause pessimistic ideation and suicidal behavior.
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Neurocognitive progression in AD can induce subsequent neuropsychiatric problems via functional reductions, complex mechanisms, and poor self-awareness.
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Interpersonal and non-pharmacological interventions are first-line approaches for reducing NPS severity in dementia.
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Patient relocation into specialized care units with appropriate facilities and staff can improve treatment-resistant NPSs in AD.
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Augmentation or combination therapy with antidepressants or antipsychotics may be helpful for treating depressive mood in AD patients with psychosis.
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Neuromodulation, including electric convulsive therapy and transcranial magnetic stimulation, may be effective alternative treatments for AD patients with apathy or depression.
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The placebo effect on NPS in AD patients can be significant, and the severity of main NPS sub-symptoms can be reduced by almost half in long-term treatment courses.
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Long-term treatment strategies based on neurocognitive mechanisms should be considered for p-TRENS-AD, and an exit strategy should be discussed.Reduction of Neuropsychiatric Symptoms in Alzheimer's Disease
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Main neuropsychiatric symptoms (NPS) in Alzheimer's disease (AD) include psychosis, agitation, and depression.
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In the CATIE-AD trial, continuation of antipsychotic drugs for treatment of psychosis or agitation was deemed unfavorable in AD patients.
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Overall severity of NPS, based on Neuropsychiatric Inventory (NPI) score, decreased by 50% after 36 weeks, including both active and placebo groups.
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Placebo group in CATIE-AD trial experienced a decrease in NPI score from 27.5 ± 17.1 to 11.6 ± 12.6 points.
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Two large randomized controlled trials (RCTs) investigating the effects of antidepressants on depression, anxiety, and agitation have shown reductions in placebo groups.
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Reductions in agitation in placebo groups were about 60-90% at 9 weeks, and reductions in depression were about 63% at 39 weeks.
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Severity of NPS may decrease in a "time-dependent manner" regardless of medication intake.
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NPS sub-symptoms require different treatments, such as mood stabilizers for bipolar symptoms, antipsychotics for hallucinations and delusions, and antidepressants for depression and anxiety.
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Studies have shown that non-pharmacological interventions, such as music therapy and behavioral interventions, can also be effective in reducing NPS.
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It is important to consider potential side effects and risks of medications when treating NPS in AD patients.
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The reduction of NPS can lead to improved quality of life for both patients and caregivers.
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More research is needed to better understand the underlying mechanisms of NPS in AD and to develop more effective treatments.
Strategies for Treating Treatment-Resistant Neuropsychiatric Symptoms in Alzheimer's Disease
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Neglecting psychosocial and demographic factors may hinder treatment response to pharmacological interventions for neuropsychiatric symptoms (NPS) in Alzheimer's disease (AD).
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Gender differences in AD patients can influence the presence of cohabitant and marital status, which may be associated with loneliness and other life changes.
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Neurocognitive mechanisms in AD can cause complex NPS sub-symptoms, including apathy, disinhibition, and depression, hindering targeted treatment.
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The severity and frequency of cognitive decline in AD patients can influence NPS sub-symptoms and treatment response.
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Poor self-awareness of cognitive symptoms and NPS in AD can lead to refusal of care and delay treatment intervention, while preserved self-awareness can cause pessimistic ideation and suicidal behavior.
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Neurocognitive progression in AD can induce subsequent neuropsychiatric problems via functional reductions, complex mechanisms, and poor self-awareness.
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Interpersonal and non-pharmacological interventions are first-line approaches for reducing NPS severity in dementia.
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Patient relocation into specialized care units with appropriate facilities and staff can improve treatment-resistant NPSs in AD.
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Augmentation or combination therapy with antidepressants or antipsychotics may be helpful for treating depressive mood in AD patients with psychosis.
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Neuromodulation, including electric convulsive therapy and transcranial magnetic stimulation, may be effective alternative treatments for AD patients with apathy or depression.
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The placebo effect on NPS in AD patients can be significant, and the severity of main NPS sub-symptoms can be reduced by almost half in long-term treatment courses.
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Long-term treatment strategies based on neurocognitive mechanisms should be considered for p-TRENS-AD, and an exit strategy should be discussed.Reduction of Neuropsychiatric Symptoms in Alzheimer's Disease
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Main neuropsychiatric symptoms (NPS) in Alzheimer's disease (AD) include psychosis, agitation, and depression.
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In the CATIE-AD trial, continuation of antipsychotic drugs for treatment of psychosis or agitation was deemed unfavorable in AD patients.
-
Overall severity of NPS, based on Neuropsychiatric Inventory (NPI) score, decreased by 50% after 36 weeks, including both active and placebo groups.
-
Placebo group in CATIE-AD trial experienced a decrease in NPI score from 27.5 ± 17.1 to 11.6 ± 12.6 points.
-
Two large randomized controlled trials (RCTs) investigating the effects of antidepressants on depression, anxiety, and agitation have shown reductions in placebo groups.
-
Reductions in agitation in placebo groups were about 60-90% at 9 weeks, and reductions in depression were about 63% at 39 weeks.
-
Severity of NPS may decrease in a "time-dependent manner" regardless of medication intake.
-
NPS sub-symptoms require different treatments, such as mood stabilizers for bipolar symptoms, antipsychotics for hallucinations and delusions, and antidepressants for depression and anxiety.
-
Studies have shown that non-pharmacological interventions, such as music therapy and behavioral interventions, can also be effective in reducing NPS.
-
It is important to consider potential side effects and risks of medications when treating NPS in AD patients.
-
The reduction of NPS can lead to improved quality of life for both patients and caregivers.
-
More research is needed to better understand the underlying mechanisms of NPS in AD and to develop more effective treatments.
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Description
Test your knowledge on the challenges in pharmacological treatment for neuropsychiatric symptoms in patients with dementia. This quiz covers the prevalence of dementia, the impact of neuropsychiatric symptoms on patient prognosis, the effectiveness of pharmacological interventions, and non-pharmacological alternatives. You will also learn about the pathogeneses of difficult-to-treat symptoms and the importance of a bio-psychosocial-neurocognitive model in treatment strategies. Keywords: dementia, neuropsychiatric symptoms, pharmacological treatment,