Efficacy and safety of galantamine in patients with mild to moderate Alzheimer's disease: multicentre randomised controlled trial

Wilcock, Gordon; Lilienfeld, Sean; Gaens, Els

doi:10.1136/bmj.321.7274.1445

Cited by 553 publications

(441 citation statements)

References 30 publications

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“…In one study of another cholinesterase inhibitor (galantamine), placebo-treated carriers and noncarriers showed similar cognitive decline over 6 months, 14 while in another similar study carriers showed greater deterioration than noncarriers. 15 A tacrine study that demonstrated less cognitive decline in APOE e4 carriers than in noncarriers, especially in women, over 30 weeks, 16 was consistent with the current 6-month rivastigmine study which shows a tendency for noncarriers taking placebo to have a greater cognitive decline than carriers. The source of these disparate results is not known.…”

Section: Discussionsupporting

confidence: 66%

Differential qualitative responses to rivastigmine in APOE ɛ4 carriers and noncarriers

et al. 2004

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This retrospective analysis of two double-blind, placebo-controlled studies in patients with mild to moderately severe AD investigated the efficacy of rivastigmine 6-12 mg/day on cognitive outcomes in patients with or without the apolipoprotein (APOE) e4 allele. APOE data were collected from patients who consented to pharmacogenetic testing. Treatment differences within each subgroup were compared, using the Observed Case (OC) population. The APOE e4 and non-APOE e4 subgroups comprised 246 and 121 patients, respectively. Overall, APOE e4 noncarriers showed greater decline than carriers (Po0.05). However, at 26 weeks, placebo-treated APOE e4 patients declined 3.04 points below baseline on the cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog), and rivastigmine-treated patients improved by 1.67 points. Non-APOE e4 placebo-treated patients declined by 4.59 points and rivastigmine-treated patients declined by 0.48 points. Thus, non-APOE e4 carriers showed a less favorable course under either placebo or rivastigmine, but both genotype-defined subgroups showed quantitatively similar responses to therapy (both Po0.05 vs placebo).

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Section: Discussionsupporting

confidence: 66%

Differential qualitative responses to rivastigmine in APOE ɛ4 carriers and noncarriers

et al. 2004

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“…In both cases this leads to an augmentation in the availability of the neurotransmitter acetylcholine. They are attributed with a 'significant, although modest, effect on the cognitive status of patients with AD' (Grutzlender and Morris, 2001), and include the plant-(snowdrop and daffodil bulb) derived drug galantamine (Wilcock et al, 2000). However, these alkaloid drugs can be toxic, offering a narrow therapeutic window, and are often associated with a number of deleterious side effects.…”

Section: Discussionmentioning

confidence: 99%

Effects of Cholinesterase Inhibiting Sage (Salvia officinalis) on Mood, Anxiety and Performance on a Psychological Stressor Battery

Kennedy

Pace

Haskell

et al. 2005

Neuropsychopharmacol

120

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Salvia officinalis (sage) has previously been shown both to possess in vitro cholinesterase inhibiting properties, and to enhance mnemonic performance and improve mood in healthy young participants. In this double-blind, placebo-controlled, crossover study, 30 healthy participants attended the laboratory on three separate days, 7 days apart, receiving a different treatment in counterbalanced order on each occasion (placebo, 300, 600 mg dried sage leaf). On each day mood was assessed predose and at 1 and 4 h postdose. Each mood assessment comprised completion of Bond-Lader mood scales and the State Trait Anxiety Inventory (STAI) before and after 20 min performance of the Defined Intensity Stress Simulator (DISS) computerized multitasking battery. In a concomitant investigation, an extract of the sage leaf exhibited dose-dependent, in vitro inhibition of acetylcholinesterase and, to a greater extent, butyrylcholinesterase. Both doses of sage led to improved ratings of mood in the absence of the stressor (that is, in pre-DISS mood scores) postdose, with the lower dose reducing anxiety and the higher dose increasing 'alertness', 'calmness' and 'contentedness' on the Bond-Lader mood scales. The reduced anxiety effect following the lower dose was, however, abolished by performing the DISS, with the same dose also being associated with a reduction of alertness during performance. Task performance on the DISS battery was improved for the higher dose at both postdose sessions, but reduced for the lower dose at the later testing session. The results confirm previous observations of the cholinesterase inhibiting properties of S. officinalis, and improved mood and cognitive performance following the administration of single doses to healthy young participants.

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“…[16][17][18][19][20] Several studies did not find that APOE genotype influenced treatment response. [21][22][23][24][25][26][27][28] Gender, either alone or in interaction with APOE genotype, was not found to influence response to ChEIs. 18,23,26,27 Several lines of evidence indicate that butyrylcholinesterase (BuChE) has a significant role in cholinergic function, both in the normal brain and in AD.…”

Section: Introductionmentioning

confidence: 99%

Effect of apolipoprotein E and butyrylcholinesterase genotypes on cognitive response to cholinesterase inhibitor treatment at different stages of Alzheimer's disease

2010

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Efficacy and safety of galantamine in patients with mild to moderate Alzheimer's disease: multicentre randomised controlled trial

Abstract: Objective To evaluate the efficacy and safety of galantamine in the treatment of Alzheimer's disease.

Cited by 553 publications

References 30 publications

Differential qualitative responses to rivastigmine in APOE ɛ4 carriers and noncarriers

Differential qualitative responses to rivastigmine in APOE ɛ4 carriers and noncarriers

Effects of Cholinesterase Inhibiting Sage (Salvia officinalis) on Mood, Anxiety and Performance on a Psychological Stressor Battery

Effect of apolipoprotein E and butyrylcholinesterase genotypes on cognitive response to cholinesterase inhibitor treatment at different stages of Alzheimer's disease

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