{"title":"Efficacy and Tolerability of a Combination Treatment of Memantine and Donepezil for Alzheimer's Disease: A Literature Review Evidence.","authors":"Mario Riverol, Andrea Slachevsky, Oscar L López","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Two types of drugs have been approved for the symptomatic treatment of Alzheimer's disease (AD): the cholinesterase inhibitors (ChEIs) and memantine. There is a growing interest to know whether the combination of these drugs is safe and if it adds any clinical benefit to patients.</p><p><strong>Objective: </strong>To systematically review published medical literature assessing the efficacy and tolerability of a combination treatment of memantine and donepezil in AD patients.</p><p><strong>Methods: </strong>We searched PubMed for English and Spanish-language literature, using the terms \"Alzheimer's disease,\" \"cholinesterase inhibitors,\" \"donepezil,\" and \"memantine.\" Our review focused on clinical trials and observational studies.</p><p><strong>Results: </strong>Eleven publications representing seven unique studies were selected for this review. Three were randomized double-blind, placebo-controlled trials and four were observational studies.</p><p><strong>Conclusions: </strong>Available data revealed that the combination of memantine and donepezil slowed down cognitive decline, prolonged functional independence, and improved behavioral symptoms in patients with moderate to severe AD. The long-term use of the dual therapy decreased the risk of nursing home admission. More longitudinal studies are needed to further examine the role of combined therapy in the management of AD patients.</p>","PeriodicalId":89550,"journal":{"name":"European neurological journal","volume":"3 1","pages":"15-19"},"PeriodicalIF":0.0,"publicationDate":"2011-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4188475/pdf/nihms330859.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32734705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Frontal and periventricular brain white matter lesions and cortical deafferentation of cholinergic and other neuromodulatory axonal projections.","authors":"N I Bohnen, C W Bogan, M L T M Müller","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>White matter fiber bundles form a spatial pattern defined by anatomical and functional architecture. Structural lesions in the white matter may cause clinical symptoms because of disruption of fiber tracts. The clinical significance will depend on the anatomic location of such lesions and whether the functional integrity of specific fiber bundles is affected. Unlike more acute lesions of stroke or multiple sclerosis that may cause sudden sensorimotor deficits, white matter lesions of aging manifest with more subtle and gradual symptoms that are often cognitive in nature. Such cognitive symptoms have been explained by strategically located white matter lesions in the deep forebrain that may disrupt cholinergic projection fibers at their proximal origin. Recent in vivo imaging studies provide supportive evidence that periventricular white matter lesions are associated with cortical cholinergic deafferentation in elderly with leukoaraiosis. White matter lesions at the frontal horns, so-called \"capping,\" are in close proximity to cholinergic axons that originate in the basal forebrain. Therefore, these lesions may result in more significant cortical deafferentation because of the more proximal axonal disruption. A unique anatomic feature common to all cortical projections from subcortical neuromodulator systems (that not only include the cholinergic but also the monoaminergic systems, such as dopamine, serotonin, and norepinephrine) is that the proximal axons largely pass through the deep forebrain before fanning out to the cortex. It is thus plausible that deep frontal white matter lesions may result in not only cholinergic but also variable monoaminergic cortical deafferentation.</p>","PeriodicalId":89550,"journal":{"name":"European neurological journal","volume":"1 1","pages":"33-50"},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387993/pdf/nihms383197.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30741017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}