Persistent treatment with cholinesterase inhibitors and/or memantine slows clinical progression of Alzheimer disease

Rountree, Susan; Chan, Wenyaw; Pavlik, Valory N.; Darby, Eveleen; Siddiqui, Samina; Doody, Rachelle S.

doi:10.1186/alzrt7

Cited by 161 publications

(116 citation statements)

References 40 publications

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“…In addition, some long-term observations suggest less decline in patients treated with AChE-Is or combination therapy of AChE-Is with memantine compared to P.S. Aisen et al patients not receiving therapy with these agents (Lopez et al 2009;Rountree et al 2009). Other clinical and imaging studies, however, suggest no disease-modifying benefit from treatment with AChE-Is (Jack et al 2008;Schneider and Sano 2009).…”

Section: Symptomatic and Other Treatments For Alzheimer Diseasementioning

confidence: 99%

Symptomatic and Nonamyloid/Tau Based Pharmacologic Treatment for Alzheimer Disease

Aisen

Cummings

Schneider

2011

Cold Spring Harbor Perspectives in Medicine

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In this work we consider marketed drugs for Alzheimer disease (AD) including acetylcholinesterase inhibitors (AChE-Is) and antiglutamatergic treatment involving the N-methyl-D-aspartate (NMDA) receptor. We discuss medications and substances available for use as cognitive enhancers that are not approved for AD or cognitive impairment, and other neurotransmitter-related therapies in development or currently being researched. We also review putative therapies that aim to slow disease progression by mechanisms not directly related to amyloid or tau. REGULATORY LANDSCAPE AND CLINICAL TRIALS

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Section: Symptomatic and Other Treatments For Alzheimer Diseasementioning

confidence: 99%

Symptomatic and Nonamyloid/Tau Based Pharmacologic Treatment for Alzheimer Disease

Aisen

Cummings

Schneider

2011

Cold Spring Harbor Perspectives in Medicine

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“…It also finds that combined treatment is superior to monotherapy. A previous large scale investigation [8] found that patients on continuous anti-dementia treatment lived three years longer, on average, than those who had no treatment or interrupted medication. Add to this a finding from residential care settings [9] documenting better function in patients taking anti-dementia medication, including a reduced need for antipsychotic medications that carry an FDA "black-box" warning.…”

Section: We Concur and Here Is Whymentioning

confidence: 99%

Dementia Screening: Saying No to the USPSTF and Yes to Brief Cognitive Evaluation

Clionsky¹

2014

J Alzheimers Dis Parkinsonism

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Recently, the U.S. Preventive Services Task Force [1] released a widely-publicized review advocating against screening for dementia in older adults. After their review of the literature, they concluded that dementia screening did no harm, but likely did little good. Their position was not based on evidence demonstrating negative outcomes for screening, as they were unable to find any particularly relevant studies that addressed the outcomes question directly. Nor was it based on significant medical risks arising from dementia treatments. They cited the common side effects of cholinesterase inhibitors and memantine, which have been known for decades and are surprisingly minimal for an old and often infirm patient population. Instead, they argued that presently available dementia treatments were not very effective. In other words, if we do not yet have good treatments, why identify the disease state?In our opinion, the USPSTF's reasoning is flawed and their conclusion is potentially harmful to patients suffering from or developing dementia. We believe that the USPSTF position leaves the public and many physicians confused about what to do and the patients with cognitive loss disenfranchised. We Concur, and Here is WhyFirst, and in rebuttal to the USPSTF assertion, the treatment picture for dementia is not as dismal as their position suggests. A contemporaneous review of the same literature [7] makes a convincing case that cholinesterase inhibitors and memantine slow cognitive and functional decline and delay nursing home placement. It also finds that combined treatment is superior to monotherapy. A previous large scale investigation [8] found that patients on continuous anti-dementia treatment lived three years longer, on average, than those who had no treatment or interrupted medication. Add to this a finding from residential care settings [9] documenting better function in patients taking anti-dementia medication, including a reduced need for antipsychotic medications that carry an FDA "black-box" warning. There are a number of single studies with similar findings which became the basis for FDA approval of dementia drugs. We can add to the clinical findings the economic benefit that treatment of dementia with donepezil reduces costs of other medical services [10].But, as noted before, treatment outcome should not be the primary or the governing reason for screening of cognition. In fact, we will argue that screening should be reframed or re-conceptualized in broader terms. We propose to replace the limited concept of screening with a more robust and useful concept called "Brief Cognitive Evaluation" or BCE. Brief Cognitive EvaluationBrief Cognitive Evaluation would employ an economical, easily administered, validated, performance-based tool to produce a metric that is reliable, sensitive to change over time, and useful in broader contexts. In our view, BCE would occur during primary care visits for older patients to measure each patient's global cognitive level as it exists today, just as we measure other impor...

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“…These were studies of patients whose treatments had been extended after completing the three-and six-month pharmaceutical company-sponsored registration trials (Doody et al, 2001;Geldmacher et al, 2003;Pirttilä et al, 2004;Raskind et al, 2004;Small et al, 2005;Burns et al, 2007;Feldman et al, 2009;Kavanagh et al, in press), and of patients tracked in academic and research clinics (GilletteGuyonnet et al, 2006;Atri et al, 2008;Lopez et al, 2009;Rountree et al, 2009). In these studies, patients continuing medications were compared to patients who had never been treated, used the drugs only briefly, or had dropped out of the randomized trials for one reason or another; some of the studies also used "projected" data from placebo patients, or historical data.…”

Section: Long-term Studies Of Cholinesterase Inhibitorsmentioning

confidence: 99%

Could cholinesterase inhibitors be harmful over the long term?

Schneider¹

2011

Int. Psychogeriatr.

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Given the rather modest clinical effects of cholinesterase inhibitors, an important question is: For how long should they be prescribed? The clinical trials that supported marketing of the drugs were only 3–6 months in duration. A couple of 12-month, placebo-controlled donepezil trials showed some advantage for Mini-Mental State Examination (MMSE) scores and maintaining a level of activities of daily living (ADL) function during that interval (Mohs et al., 2001; Winblad et al., 2001). The controversial AD2000 trial in the UK tended to show MMSE and ADL efficacy over at least two years (Courtney et al., 2004), but the authors questioned whether treatment was worthwhile or cost-effective.

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Persistent treatment with cholinesterase inhibitors and/or memantine slows clinical progression of Alzheimer disease

Cited by 161 publications

References 40 publications

Symptomatic and Nonamyloid/Tau Based Pharmacologic Treatment for Alzheimer Disease

Symptomatic and Nonamyloid/Tau Based Pharmacologic Treatment for Alzheimer Disease

Dementia Screening: Saying No to the USPSTF and Yes to Brief Cognitive Evaluation

Could cholinesterase inhibitors be harmful over the long term?

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