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Anticholinergics and benzodiazepines on cognitive impairment among elderly with Alzheimer's disease: a 1 year follow-up study.

ABSTRACT: OBJECTIVE:Age-associated decline in central cholinergic activity makes older adults susceptible to harmful effects of anticholinergics (ACs). Evidence exists of an association between effects of AC medications on cognition. This retrospective cohort study examines how ACs affect cognition among older adults with Alzheimer's disease (AD) who received acetylcholine esterase inhibitors (AChEIs) over the course of 12 months. RESULTS:A total of 133 (80% women, mean age 78.38 years, SD 7.4) were recruited. No difference in sex, age and comorbid diseases was observed between participants who took ACs, benzodiazepines (BZDs) and AChEIs. The most common prescribed ACs was quetiapine, being used for behavioral and psychological symptoms (BPSD). Multilevel analysis showed that the change of mental state examination scores were significantly predicted in the group using ACs (t (169), -?2.52, p?=?.020) but not with the groups using BZD (t (162), 0.84, p?=?.440). Evidence showed that older adults with Alzheimer's disease and exposed to ACs exhibited lower global cognitive scores than those without AC exposure. Using ACs could be a trade-off between controlling BPSD and aggravating cognitive impairment. Highlighting the awareness of the potential anticholinergic effect is important and may be the best policy.

SUBMITTER: Jenraumjit R

PROVIDER: S-EPMC6941288 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Anticholinergics and benzodiazepines on cognitive impairment among elderly with Alzheimer's disease: a 1 year follow-up study.

Jenraumjit Rewadee R Chinwong Surarong S Chinwong Dujrudee D Kanjanarach Tipaporn T Kshetradat Thanat T Wongpakaran Tinakon T Wongpakaran Nahathai N

BMC research notes 20200102 1

<h4>Objective</h4>Age-associated decline in central cholinergic activity makes older adults susceptible to harmful effects of anticholinergics (ACs). Evidence exists of an association between effects of AC medications on cognition. This retrospective cohort study examines how ACs affect cognition among older adults with Alzheimer's disease (AD) who received acetylcholine esterase inhibitors (AChEIs) over the course of 12 months.<h4>Results</h4>A total of 133 (80% women, mean age 78.38 years, SD ...[more]

PMID: 31898553

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Project description:IntroductionBiomarkers that will reliably predict the onset of Alzheimer's disease (AD) are urgently needed. Although cerebrospinal fluid (CSF) amyloid beta 1-42 (A?42), total tau, and phosphorylated tau can be used to complement the clinical diagnosis of AD, amnestic mild cognitive impairment (aMCI), the prodromal phase of AD, is heterogeneous. Biomarkers should be able to determine which patients with aMCI are at greatest risk of AD. Histological studies and animal models indicate that amyloid beta 1-43 (A?43) aggregates early, and may play a role in the pathological process of AD. We have examined levels of CSF A?43 in a 2-year longitudinal study of aMCI and early AD.Materials and methodsCerebrospinal fluid was collected at baseline, and after one and 2 years from patients with AD (n = 19), and patients with aMCI (n = 42). Of these, 21 progressed to AD during the 2 years of study, whereas 21 did not. Controls (n = 32) were lumbar punctured at baseline only. CSF analyses of A?43, A?42, and total tau were carried out with ELISA.ResultsAt baseline, CSF A?43, CSF A?42 and ratios with total tau could be used to separate controls from all three patient groups. CSF A?43, but not A?42, could separate patients with aMCI who progressed to AD during the 2 years of follow-up, from those that did not. The CSF total tau/A?43 ratio had a slightly but significantly larger area under the receiver operating characteristic curve when compared to the CSF total tau/A?42 ratio. CSF A?43 levels, but not A?42 levels, decreased from baseline to 2 years in the AD group.Discussion and conclusionCSF A?43 was demonstrated to be significantly reduced in patients already by the time that aMCI or AD was diagnosed, compared to controls, and this change must have occurred during the preclinical period. Since our results suggested that CSF A?43 distinguishes between subgroups of patients with aMCI better than CSF A?42, it may prove to be a useful additional biomarker for identifying aMCI patients at greatest risk of AD.

Project description:This study investigated the ability of magnetic resonance spectroscopy (1H-MRS) of posterior cingulate cortex (PCC) and brain volumetry to predict the progression from mild cognitive impairment (MCI) to Alzheimer's Disease (AD) on the basis of clinical classification at 2?years follow-up. Thirty-eight MCI patients, eighteen healthy older adults and twenty-three AD patients were included in this study. All participants underwent a brain-MR protocol (1.5?T GE scanner) including high-resolution T1-weighted volumetric sequence (isotropic 1mm3). Voxel-wise differences in brain volumetry were evaluated using FreeSurfer software and all volumes were normalized by the total intracranial volume (TIV). Careful localization of 1H-MRS volume of PCC was performed and data were processed with the LCModel program. MCI patients underwent a complete neuropsychological assessment at baseline and were clinically re-evaluated after a mean of 28?months; twenty-six MCI patients (68.4%) converted to AD and twelve remained stable. At baseline these two MCI subgroups did not differ in the global cognitive level (Mini Mental State Examination, MMSE) or in any of the other cognitive domains; the NAA/ mI ratio in the PCC was able to differentiate MCI converters from those MCI that did not develop AD (p?=?0.022) with a level of accuracy (AUC area) of 0.779. A significantly reduced volume of parahippocampal gyrus (p?=?0.010) and fusiform gyrus (p?=?0.026) were found in the converter MCI subgroup compared to the stable MCI subgroup. The combined use of both N- acetyl-aspartate (NAA)/myo-Inositol (mI) ratio and volume of parahippocampal gyrus, increases the overall accuracy (AUC?=?0.910) in predicting the conversion to AD two years before the development of clinical symptoms. Additional longitudinal studies with a broader representative sample of MCI patients and longer follow-up might be helpful to confirm these results and to elucidate the role of each parameter in predicting the possible progression to AD, and also to all the other non-AD dementia subtypes.

Project description:BACKGROUND:Control of vascular risk factors is essential for secondary stroke prevention. However, adherence to secondary prevention medications is often suboptimal, and may be affected by cognitive impairment. Few studies to date have examined associations between cognitive impairment and medication adherence post-stroke, and none have considered whether adherence to secondary prevention medications might affect subsequent cognitive function. The aim of this study was to explore prospective associations between cognitive impairment and medication non-adherence post-stroke. METHODS:A five-year follow-up of 108 stroke survivors from the Action on Secondary Prevention Interventions and Rehabilitation in Stroke (ASPIRE-S) prospective observational cohort study. Cognitive function was assessed using the Montreal Cognitive Assessment at 6 months, and a neuropsychological test battery at 5 years. Adherence to antihypertensive, antithrombotic and lipid-lowering medications was assessed using prescription refill data. RESULTS:The prevalence of cognitive impairment at five years was 35.6%. The prevalence of non-adherence ranged from 15.1% for lipid-lowering agents to 30.2% for antithrombotics. There were no statistically significant associations between medication non-adherence in the first year post-stroke and cognitive impairment at 5 years, nor between cognitive impairment at 6 months and non-adherence at 5 years. Stroke survivors with cognitive impairment were significantly more likely to report receiving help with taking medications [OR (95% CI): 4.84 (1.17, 20.07)]. CONCLUSIONS:This is the first study to explore the potential impact of non-adherence to secondary prevention medications on cognitive impairment in stroke survivors. Findings highlight the role of family members and caregivers in assisting stroke survivors with medication administration, particularly in the context of deficits in cognitive function. Involving family members and caregivers may be a legitimate and cost-effective strategy to improve medication adherence in stroke survivors.

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Anticholinergics and benzodiazepines on cognitive impairment among elderly with Alzheimer's disease: a 1 year follow-up study.

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Anticholinergics and benzodiazepines on cognitive impairment among elderly with Alzheimer's disease: a 1 year follow-up study.

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