Galantamine for vascular cognitive impairment

Whitla Medical Building, School of Medicine and Dentistry, Queen's University of Belfast, 97 Lisburn Road, Belfast, UK, BT9 7BL.
Cochrane database of systematic reviews (Online) (Impact Factor: 6.03). 01/2006; 1(1):CD004746. DOI: 10.1002/14651858.CD004746.pub2
Source: PubMed


The efficacy of galantamine has been tested in two randomised controlled trials for the treatment of vascular dementia and for a mixed population of Alzheimer's disease patients with evidence of cerebrovascular disease on scanning. The rationale behind its use is to correct the cholinergic deficit seen in vascular dementia. This review found evidence of benefit for galantamine compared with placebo in measures of cognition in both studies. Both studies indicated higher rates of nausea and vomiting in patients taking galantamine compared with placebo.

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    • "Encouraging results of galantamine monotherapy for ASD treatment have been reported in three separate studies to date (Hertzman, 2003; Nicolson et al., 2006a; Niederhofer et al., 2002), and numerous investigations suggest that there are beneficial effects for this agent in treating other serious neuropsychiatric disorders (Craig et al., 2006; Ghaemi et al., 2009; Litvinenko et al., 2008; Loy et al., 2006; Schubert et al., 2006). "
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    ABSTRACT: The role of cholinergic abnormalities in autism was recently evidenced and there is a growing interest in cholinergic modulation, emerging for targeting autistic symptoms. Galantamine is an acetylcholinesterase inhibitor and an allosteric potentiator of nicotinic receptors. This study aimed to evaluate the possible effects of galantamine as an augmentative therapy to risperidone, in autistic children. In this randomized, double-blind, placebo-controlled, parallel-group study, 40 outpatients aged 4-12 years whom had a diagnosis of autism (DSM IV-TR) and a score of 12 or higher on the Aberrant Behavior Checklist-Community (ABC-C) Irritability subscale were equally randomized to receive either galantamine (up to 24 mg/day) or placebo, in addition to risperidone (up to 2 mg/day), for 10 weeks. We rated participants by ABC-C and a side effects checklist, at baseline and at weeks 5 and 10. By the study endpoint, the galantamine-treated patients showed significantly greater improvement in the Irritability (P = 0.017) and Lethargy/Social Withdrawal (P = 0.005) subscales than the placebo group. The difference between the two groups in the frequency of side effects was not significant. In conclusion, galantamine augmentation was shown to be a relatively effective and safe augmentative strategy for alleviating some of the autism-related symptoms.
    Journal of Psychopharmacology 10/2013; 28(7). DOI:10.1177/0269881113508830 · 3.59 Impact Factor
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    • "The prior recommendation that singled out galantamine was based on a subgroup analysis from a RCT in those with AD and cerebrovascular disease that was not replicated [24]. The Cochrane Review on the use of galantamine for vascular cognitive impairment concluded that 'More studies are needed before firm conclusions can be drawn' about its use [25]. "
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    ABSTRACT: While there have been no new medications approved for the treatment of Alzheimer's disease (AD) or other dementias in Canada since 2004, the Canadian Consensus Conference on the Diagnosis and Treatment of Dementia (CCCDTD) reviewed and updated the clinical practice guidelines on the pharmacological management of dementia that were published previously. This review focused on the literature for the pharmacological treatment of dementia based on studies published since the third CCCDTD in 2006. A literature search of English-language medical databases was preformed for studies pertaining to the pharmacological treatment of AD and other dementias that examined the management of cognitive and functional impairment, as well as neuropsychiatric symptoms. All previous recommendations were reviewed, and only those that required updating based on new published studies were revised. Several new recommendations were also added. Recommendations were rated for quality of evidence and were approved by consensus. There were 15 revised or new recommendations approved by consensus. The revised recommendations included acknowledging that cholinesterase inhibitors (ChEIs) possess a class effect and any of the agents can be used for AD across the spectrum of severity and with co-existing cerebrovascular disease. There was insufficient evidence to recommend for or against the use of ChEIs in combination with memantine for the primary indication of treating neuropsychiatric symptoms, or for the treatment of vascular dementia. Recommendations for the discontinuation of cognitive enhancers were revised and clarified, as well as the risks associated with discontinuing these drugs. ChEIs were recommended as a treatment option for dementia with Parkinson's disease. Risks associated with use of antipsychotics for neuropsychiatric symptoms were strengthened, and guidelines regarding the use of antidepressants for affective disturbances in dementia were weakened, and are now considered an option but not a firm recommendation. Valproate was recommended not to be used, and there was insufficient evidence to recommend for or against the use of selective serotonin reuptake inhibitors or trazodone for the treatment of agitation and aggression. In spite of the lack of new therapeutic agents for the treatment of dementia, recent studies have helped to clarify and strengthen recommendations to optimize the pharmacological management of these illnesses.
    Alzheimer's Research and Therapy 07/2013; 5(Suppl 1):S5. DOI:10.1186/alzrt201 · 3.98 Impact Factor
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    • "At 26 weeks, there were improvements in galantamine-treated patients at doses of 16 mg to 24 mg per day. However, a significant percentage of patients dropped out owing to adverse events, particularly gastrointestinal effects.33,34 "
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    ABSTRACT: Cerebrovascular disease is the second leading cause of cognitive impairment in the elderly, either alone or in combination with Alzheimer's disease (AD). Vascular dementia (VaD) is heterogeneous in terms of both clinical phenotype and pathogenetic mechanisms. It may result from multiple cortical infarctions due to cerebral large vessel pathologies or to subcortical ischemic changes such as leukoaraiosis or lacunar infarction due to cerebral small artery disease. Clinical symptoms and signs vary depending on the location and size of the stroke lesion, and no single neuropsychological profile characteristic of VaD has been defined, although dysexecutive function is common. A slightly higher mortality rate and slower progression are reported in VaD compared with AD. VaD is potentially preventable by rigorous identification and treatment of cardiovascular disease risk factors, and modest symptomatic improvement with cholinesterase inhibitors has been reported.
    08/2011; 47(2):66-71. DOI:10.4068/cmj.2011.47.2.66
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