The feed additive ractopamine, a β-adrenergic agonist, has been approved for use in livestock for nearly 2 decades. Studies of its possible adverse effects in humans have concentrated exclusively on cardiovascular disease and cardiovascular functional disorders in the past. In this article, whether and how ractopamine may affect neurodegeneration, either to promote or to reduce the incidence of Alz-heimer disease, will be discussed based on the recent controversial findings that β-adrenoreceptor activation not only can stimulate Alzheimer-pathogenic amyloid-β accumulation but also are able to enhance hippocampal neurogenesis and ameliorate mouse memory deficits in independent laboratory studies. Furthermore, environmental enrichment has been found to prevent impairment of memory-related hippocampal long-term potentiation and microglia-mediated neuroinflammation induced by amyloid-β. These beneficial effects are achieved mainly through enhanced β-adrenergic signaling and can be imitated by β agonist isoprotenerol. Finally, it has been demonstrated that the β-adrenergic agonist salbutamol could bind directly to tau protein and interfere with the tau filament formation seen in the prodromal phase of Alzheimer disease. These complex but interesting issues lead to contradictory speculations of possible effects of ractopamine residue in meat on Alzheimer disease. Hypotheses derived from this review surely deserve carefully designed laboratory investigations and clinical studies in the future.
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http://dx.doi.org/10.1159/000515677 | DOI Listing |
Int J Surg
January 2025
Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Introduction: Lung function has been associated with cognitive decline and dementia, but the extent to which lung function impacts brain structural changes remains unclear. We aimed to investigate the association of lung function with structural macro- and micro-brain changes across mid- and late-life.
Methods: The study included a total of 37 164 neurologic disorder-free participants aged 40-70 years from the UK Biobank, who underwent brain MRI scans 9 years after baseline.
Neurochem Res
January 2025
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder characterized by cognitive decline. Despite extensive research, therapeutic options remain limited. Varenicline, an αβ nicotinic acetylcholine receptor agonist, shows promise in enhancing cognitive function.
View Article and Find Full Text PDFHum Brain Mapp
February 2025
Department of Neurology, Washington University in St. Louis, St. Louis, Missouri, USA.
Neurodegeneration is presumed to be the pathological process measure most proximal to clinical symptom onset in Alzheimer Disease (AD). Structural MRI is routinely collected in research and clinical trial settings. Several quantitative MRI-based measures of atrophy have been proposed, but their low correspondence with each other has been previously documented.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Pathology & Laboratory Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA.
Alzheimers Dement
January 2025
Center for Motor Neuron Biology and Disease, Columbia University Medical Center, New York, New York, USA.
This proceedings article summarizes the inaugural "T Cells in the Brain" symposium held at Columbia University. Experts gathered to explore the role of T cells in neurodegenerative diseases. Key topics included characterization of antigen-specific immune responses, T cell receptor (TCR) repertoire, microbial etiology in Alzheimer's disease (AD), and microglia-T cell crosstalk, with a focus on how T cells affect neuroinflammation and AD biomarkers like amyloid beta and tau.
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