Sleep Science Abstracts
1. Pharmacol Biochem Behav. 2011 Oct;99(4):704-11. Epub 2011 Jul 1.
Melatonin protects against neurobehavioral and mitochondrial deficits in a chronic mouse model of Parkinson’s disease.
Source
Department of Pharmacological and Pharmaceutical Sciences, University of Houston, TX, USA.
Abstract
Neuronal oxidative stress and mitochondrial dysfunction are implicated in Parkinson’s disease. Melatonin, a natural antioxidant, was shown to reduce oxidative stress and protect mitochondrial functions. This study evaluated long-term melatonin treatment on mitochondrial and dopaminergic functions, as well as locomotor performance, in a chronic mouse model of Parkinson’s disease. Chronic Parkinsonian mice pre-treated with melatonin (5mg/kg/day) for 18 weeks showed full preemption of mitochondrial respiratory defects, ATP, and antioxidant enzyme deficits. Striatal dopaminergic and locomotor deficits were significantly mitigated. These findings suggest that melatonin may slow the progression of Parkinson’s disease and reduce oxidative stress in mitochondrial disorders.
2. Int J Dev Neurosci. 2008 Oct;26(6):585-91. Epub 2008 May 9.
Protective role of melatonin on PCB (Aroclor 1,254) induced oxidative stress and changes in ATPases in rat brain.
Venkataraman P, Krishnamoorthy G, et al.
Source
Department of Endocrinology, University of Madras, Chennai, India.
Abstract
Polychlorinated biphenyls (PCBs) are environmental neurotoxins that induce oxidative stress and alter ion gradients across membranes. This study evaluated melatonin’s protective role against PCB-induced changes in brain ATPase activity and oxidative stress. PCB-treated rats showed increased lipid peroxidation, H2O2, and hydroxyl radicals, alongside decreased antioxidant enzyme activity. Melatonin supplementation restored these parameters, demonstrating its neuroprotective potential against environmental toxins.
3. Prog Neurobiol. 1998 Oct;56(3):359-84.
Oxidative damage in the central nervous system: protection by melatonin.
Source
Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, USA.
Abstract
Melatonin, an effective free radical scavenger, protects against oxidative damage in neurological diseases. It scavenges hydroxyl radicals, peroxynitrite, and peroxyl radicals while enhancing antioxidative enzyme activity. Melatonin reduces oxidative stress in Parkinson’s, Alzheimer’s, and other neurodegenerative disease models. Its decline with age may contribute to increased neurodegenerative risk, underscoring its therapeutic potential.
4. J Neurosci. 1997 Mar 1;17(5):1683-90.
Melatonin prevents death of neuroblastoma cells exposed to the Alzheimer amyloid peptide.
Pappolla MA, et al.
Source
Department of Pathology and Laboratory Medicine, University of South Alabama, Mobile, USA.
Abstract
Melatonin effectively prevented oxidative damage and cell death in neuroblastoma cells exposed to Alzheimer amyloid peptides. The findings suggest melatonin's therapeutic relevance in Alzheimer’s disease, particularly due to its antioxidant properties and its decline with aging.
5. Life Sci. 1997;60(2):PL23-9.
Melatonin is protective against MPTP-induced striatal and hippocampal lesions.
Acuña-Castroviejo D, et al.
Source
Instituto de Biotecnologia, Universidad de Granada, Spain.
Abstract
In a Parkinson’s disease mouse model, melatonin reversed lipid peroxidation in the striatum and hippocampus and protected nerve terminals. This highlights melatonin’s potential as a neuroprotective agent against neurodegenerative disorders.
6. Exp Gerontol. 1995 May-Aug;30(3-4):199-212.
The pineal gland and melatonin in relation to aging: a summary of theories and data.
Source
Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, USA.
Abstract
Melatonin’s decline with age may dysregulate circadian rhythms and accelerate aging. As a potent antioxidant, melatonin protects against oxidative stress, potentially mitigating aging and age-related neurodegeneration.
