Assessing the Possible Influence of Residues of Ractopamine, a Livestock Feed Additive, in Meat on Alzheimer Disease

Abstract

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 Alz­heimer 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.

Keywords

• alzheimer disease
• ractopamine
• amyloid-β
• tau protein
• neurogenesis
• neuroinflammation