Llanquinao Jesús, Jara Claudia, Cortés-Díaz Daniela, Kerr Bredford, Tapia-Rojas Cheril
Laboratory of Neurobiology of Aging, Centro de Biología Celular y Biomedicina (CEBICEM), Facultad de Medicina y Ciencia, Universidad San Sebastián, Providencia-Santiago 7510157, Chile.
Laboratory of Neuroendocrinology and Metabolism, Centro de Biología Celular y Biomedicina (CEBICEM), Facultad de Medicina y Ciencia, Universidad San Sebastián, Providencia-Santiago 7510157, Chile.
Neurol Int. 2024 Sep 23;16(5):1066-1085. doi: 10.3390/neurolint16050080.
Aging has been extensively studied, with a growing interest in memory impairment by a neurobiological approach. Mitochondrial dysfunction is a hallmark of aging, contributing to the aging phenotype; therefore, mitochondrial interventions seem fundamental. The diet is a physiological approximation for modifying mitochondria, which could impact the age-related phenotype. We studied two diets with low-carbohydrate and high-fat compositions, differing in the amount of protein and the fat type disposable-the atherogenic diet Cocoa (high protein/high saturated fat/high cholesterol) and the South Beach diet (very high-protein/high-unsaturated fat)-on oxidative stress, mitochondrial state, and hippocampus-dependent memory in 3-month-old Senescence-Accelerated Mouse Model (SAMP8) seed over 3 months to determine their pro- or anti-aging effects. Despite its bad reputation, the Cocoa diet reduces the reactive oxygen species (ROS) content without impacting the energy state and hippocampus-dependent spatial acuity. In contrast to the beneficial impact proposed for the South Beach diet, it induced a pro-aging phenotype, increasing oxidative damage and the levels of NR2B subunit of the NMDA, impairing energy and spatial acuity. Surprisingly, despite the negative changes observed with both diets, this led to subtle memory impairment, suggesting the activation of compensatory mechanisms preventing more severe cognitive decline. Our results demonstrated that diets usually considered good could be detrimental to the onset of aging. Also, probably due to the brain plasticity of non-aged animals, they compensate for the damage, preventing a more aggravated phenotype. Nevertheless, these silent changes could predispose or increase the risk of suffering pathologies at advanced age.
衰老已得到广泛研究，人们越来越有兴趣通过神经生物学方法研究记忆障碍。线粒体功能障碍是衰老的一个标志，促成了衰老表型；因此，线粒体干预似乎至关重要。饮食是一种调节线粒体的生理途径，可能会影响与年龄相关的表型。我们研究了两种低碳水化合物和高脂肪组成的饮食，它们在蛋白质含量和可利用脂肪类型上有所不同——致动脉粥样硬化饮食可可（高蛋白/高饱和脂肪/高胆固醇）和南滩饮食（极高蛋白/高不饱和脂肪）——对3个月大的衰老加速小鼠模型（SAMP8）在3个月内的氧化应激、线粒体状态和海马依赖性记忆的影响，以确定它们的促衰老或抗衰老作用。尽管可可饮食名声不佳，但它能降低活性氧（ROS）含量，而不影响能量状态和海马依赖性空间敏锐度。与对南滩饮食提出的有益影响相反，它诱导了一种促衰老表型，增加了氧化损伤和NMDA的NR2B亚基水平，损害了能量和空间敏锐度。令人惊讶的是，尽管两种饮食都观察到了负面变化，但这导致了轻微的记忆障碍，表明激活了补偿机制以防止更严重的认知衰退。我们的结果表明，通常被认为有益的饮食可能对衰老的发生有害。此外，可能由于未衰老动物的大脑可塑性，它们能够补偿损伤，防止出现更严重的表型。然而，这些无声的变化可能会使老年时患疾病的倾向增加或风险升高。
