Maladie d’Alzheimer, traitement des troubles psychologiques et comportementaux

Pancrazi, Marie-Pierre; Métais, Pierre

doi:10.1016/s0755-4982(05)84011-4

Cited by 9 publications

(2 citation statements)

References 23 publications

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“…164 Duloxetine has improved several measures of depression and cognition in a double-blind, placebocontrolled trial in geriatric patients. 165 Experience with selective serotonin reuptake inhibitors (SSRIs) and norepinephrine reuptake inhibiting antidepressants, together with neurotransmitter correlate findings for certain neuropsychiatric disorders, suggests that duloxetine has the potential to improve depression, [165][166][167][168][169][170][171][172][173][174][175] anxiety, 15,16,166,172,176 hallucinations, [177][178][179][180][181] delusions, 177,181,182 sleep, 183,184 agitation, 166,181,182,185,186 aggression, 181,182,186 irritability, 166,176,181,182,186,187 disinhibition, 188,189 excitement, 176,182 wandering, 182 overall cognition, 165,190 -193 attention, 194 -196 executive functioning, 197 and memory 165 across neurodegenerative diseases. Apathy and urinary incontinence may also respond to duloxetine.…”

Section: Methodsmentioning

confidence: 99%

Psychopharmacological Neuroprotection in Neurodegenerative Disease: Heuristic Clinical Applications

Lauterbach¹,

Shillcutt²,

Victoroff³

et al. 2010

Journal of Neuropsychiatry

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In Part I of this report, the authors reviewed preclinical and clinical evidence of neuroprotection by psychotropics and proposed criteria to predict translational neuroprotection. Here, the authors review a broad array of neuroprotective mechanisms and, based on evidence reviewed in Part I, consider agents with pharmacodynamic mechanisms of action that may be associated with neuroprotection. The neuroprotective potential of the pharmacodynamic mechanisms discussed here are held in common with drugs that evidenced neuroprotective potential in Part I. The agents examined here have symptomatic utility in neurodegenerative disease neuropsychiatric disorders and combine the most promising pharmacodynamic mechanisms yet have received insufficient research to date. Modafinil, duloxetine, ziprasidone, s-zopiclone, and ramelteon are evaluated in terms of their putative neuropsychiatric symptomatic and heuristic neuroprotective disease-modifying potentials. The authors review these agents in terms of their potential for clinical neuroprotection and suggest a criterion-based research agenda for future studies of their neuroprotective potential. Further research is needed with regard to the 10 translational neuroprotective candidate criteria, neuroprotective clinical trials, the correlation of psychotropic pharmacodynamic mechanisms with neuroprotective actions, and the translational predictive utility of the proposed candidate criteria.

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Section: Methodsmentioning

confidence: 99%

Psychopharmacological Neuroprotection in Neurodegenerative Disease: Heuristic Clinical Applications

Lauterbach¹,

Shillcutt²,

Victoroff³

et al. 2010

Journal of Neuropsychiatry

View full text Add to dashboard Cite

show abstract

“…228,229 Donepezil may improve the symptoms in moderately severe noninstitutionalized AD but showed no efficacy in mild to moderate noninstitutionalized AD or severe institutionalized AD patients, 230 suggesting a limited window of therapeutic efficacy. Other studies showed that ChE 231,232 and AChE inhibitors 233 may improve apathy (see, however Ref. 234 for contrasting findings).…”

Section: Neurotransmitter Systems and Emotion Processing Dysfunction ...mentioning

confidence: 98%

Emotion Processing Dysfunction in Alzheimer’s Disease: An Overview of Behavioral Findings, Systems Neural Correlates, and Underlying Neural Biology

Chaudhary

Zhornitsky

Chao

et al. 2022

Am J Alzheimers Dis Other Demen

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We described behavioral studies to highlight emotional processing deficits in Alzheimer’s disease (AD). The findings suggest prominent deficit in recognizing negative emotions, pronounced effect of positive emotion on enhancing memory, and a critical role of cognitive deficits in manifesting emotional processing dysfunction in AD. We reviewed imaging studies to highlight morphometric and functional markers of hippocampal circuit dysfunction in emotional processing deficits. Despite amygdala reactivity to emotional stimuli, hippocampal dysfunction conduces to deficits in emotional memory. Finally, the reviewed studies implicating major neurotransmitter systems in anxiety and depression in AD supported altered cholinergic and noradrenergic signaling in AD emotional disorders. Overall, the studies showed altered emotions early in the course of illness and suggest the need of multimodal imaging for further investigations. Particularly, longitudinal studies with multiple behavioral paradigms translatable between preclinical and clinical models would provide data to elucidate the time course and underlying neurobiology of emotion processing dysfunction in AD.

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Current awareness in geriatric psychiatry

2005

Int. J. Geriat. Psychiatry

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Maladie d’Alzheimer, traitement des troubles psychologiques et comportementaux

Cited by 9 publications

References 23 publications

Psychopharmacological Neuroprotection in Neurodegenerative Disease: Heuristic Clinical Applications

Psychopharmacological Neuroprotection in Neurodegenerative Disease: Heuristic Clinical Applications

Emotion Processing Dysfunction in Alzheimer’s Disease: An Overview of Behavioral Findings, Systems Neural Correlates, and Underlying Neural Biology

Current awareness in geriatric psychiatry

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