Agitation is a common neuropsychiatric symptom (NPS) in the early and middle stages of Alzheimer's disease (AD) dementia, which is difficult to treat and causes much distress. The U.S. Food and Drug Administration (U.S. FDA) issued black box warnings against the use of antipsychotics in dementia in 2005 and 2008 due to the increased risk of morbidity and mortality, resulting in the reduction in antipsychotic use for treating dementia-related NPS and spurring the quest for safer and more effective pharmacological options. The data favoring the use of citalopram for treating agitation in AD dementia is particularly compelling, and this may be a class effect for all selective serotonin reuptake inhibitors. However, concerns about the cardiac side-effects of citalopram have limited its widespread use for this indication. In this article, available efficacy and safety data for the use of citalopram and escitalopram in treating agitation in AD dementia is reviewed, using a composite case to illustrate key points. Practical recommendations are made to facilitate the use of these medications in routine clinical practice, risk mitigation strategies are discussed and salient issues for future clinical research are emphasized.
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http://dx.doi.org/10.1016/j.jagp.2019.04.016 | DOI Listing |
Environ Sci Technol
March 2025
Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, Georgia 30322, United States.
Fine particulate matter (PM) is linked to dementia risk, but ultrafine particles (UFPs, <100 nm) may be even more toxic due to their distinct physicochemical properties. However, evidence on UFPs and dementia remains limited. This study assessed the association between UFP exposure and Alzheimer's disease (AD) and related dementias (ADRD) among U.
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February 2025
Center for Dementia Research, Nathan Kline Institute, Orangeburg, NY, United States.
Introduction: Individuals with Down syndrome (DS) exhibit neurological deficits throughout life including the development of in Alzheimer's disease (AD) pathology and cognitive impairment. At the cellular level, dysregulation in neuronal gene expression is observed in postmortem human brain and mouse models of DS/AD. To date, RNA-sequencing (RNA-seq) analysis of hippocampal neuronal gene expression including the characterization of discrete circuit-based connectivity in DS remains a major knowledge gap.
View Article and Find Full Text PDFDrugs Context
March 2025
Department of Psychiatry, Creighton University School of Medicine, Omaha, NE, USA.
This Editorial reviews data on the efficacy and adverse effects of lecanemab amongst individuals with mild Alzheimer disease. Additionally, the recent controversy regarding the rejection by the EMA of a marketing authorization request for lecanemab, followed by its subsequent approval, is also discussed. The need for thoughtful discussions regarding the risks and benefits of this medication as well as the importance of developing Appropriate Use Recommendations and/or national guidelines for the use of lecanemab are also highlighted.
View Article and Find Full Text PDFBackground And Aims: Alzheimer's disease (AD) is a widespread neurodegenerative condition that has a growing impact on a global scale. This study aims to examine the relationship between cerebral blood flow (CBF) and the synaptic biomarker growth-associated protein 43 (GAP-43) through the utilization of arterial spin labeling (ASL). The research identified noteworthy correlations between cerebrospinal fluid (CSF) GAP-43 levels, CBF, and cognitive composite scores, especially among participants with mild cognitive impairment (MCI) who possess the APOE-ε4 gene.
View Article and Find Full Text PDFBrain Commun
February 2025
National Dementia BioBank, AMPAEYDEN A.C., and Federación Mexicana de Alzheimer, Estado de México CP 54743, México.
Alzheimer's disease is characterized by progressive memory loss and deterioration of cognitive functions. The presence of neurofibrillary tangles in the hippocampal areas (perforant pathway) correlates with cognitive impairment. Pathological processing of tau protein is characterized by post-translational changes such as hyperphosphorylation and truncation, which favour conformational changes within tau.
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