Mark P. Mattson

Upon conducting a thorough investigation into the issue, the authors discovered that the similarity resulted from an unintentional error. Specifically, an author mistakenly selected an incorrect representative image for the Western blot (WB) results, scanning the wrong face of the same film used to generate Figure 3A, and incorrectly labeled the resulting image. The two figures in question originated from separate scans but were inadvertently taken from the same membrane.

The Topoisomerase 3B (Top3b) - Tudor domain containing 3 (Tdrd3) protein complex is the only dual-activity topoisomerase complex that can alter both DNA and RNA topology in animals. TOP3B mutations in humans are associated with schizophrenia, autism and cognitive disorders; and Top3b-null mice exhibit several phenotypes observed in animal models of psychiatric and cognitive disorders, including impaired cognitive and emotional behaviors, aberrant neurogenesis and synaptic plasticity, and transcriptional defects. Similarly, human TDRD3 genomic variants have been associated with schizophrenia, verbal short-term memory and educational attainment. However, the importance of Tdrd3 in normal brain function has not been examined in animal models. Here we generated a Tdrd3-null mouse strain and demonstrate that these mice display both shared and unique defects when compared to Top3b-null …

Animals live in habitats fraught with a range of environmental challenges to their bodies and brains. Accordingly, cells and organ systems have evolved stress-responsive signaling pathways that enable them to not only withstand environmental challenges but also to prepare for future challenges and function more efficiently. These phylogenetically conserved processes are the foundation of the hormesis principle, in which single or repeated exposures to low levels of environmental challenges improve cellular and organismal fitness and raise the probability of survival. Hormetic principles have been most intensively studied in physical exercise but apply to numerous other challenges known to improve human health (e.g., intermittent fasting, cognitive stimulation, and dietary phytochemicals). Here we review the physiological mechanisms underlying hormesis-based neuroplasticity and neuroprotection …

Huntington's disease (HD) is a dominantly inherited neurodegenerative disorder caused by a trinucleotide repeat expansion in the huntingtin gene resulting in long stretches of polyglutamine repeats in the huntingtin protein. The disease involves progressive degeneration of neurons in the striatum and cerebral cortex resulting in loss of control of motor function, psychiatric problems, and cognitive deficits. There are as yet no treatments that can slow disease progression in HD. Recent advances in gene editing using clustered regularly interspaced short palindromic repeats (CRISPR)–CRISPR-associated protein 9 (Cas9) systems and demonstrations of their ability to correct gene mutations in animal models of a range of diseases suggest that gene editing may prove effective in preventing or ameliorating HD. Here we describe (i) potential CRISPR-Cas designs and cellular delivery methods for the correction of …

The authors regret that Figure 1 included an image of 2 people trying to start a fire which was labelled as ‘Animals’ instead of ‘Humans’. We sincerely apologize for any offense caused, which was entirely unintentional. Figure 1 has been replaced with a new figure with the correct labels.Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author (s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by …

How intermittent fasting can enhance resilience, improve mental and physical performance, and protect against aging and disease. Most of us eat three meals a day with a smattering of snacks because we think that’s the normal, healthy way to eat. This book shows why that’s not the case. The human body and brain evolved to function well in environments where food could be obtained only intermittently. When we look at the eating patterns of our distant ancestors, we can see that an intermittent fasting eating pattern is normal—and eating three meals a day is not. In The Intermittent Fasting Revolution, prominent neuroscientist Mark Mattson shows that intermittent fasting is not only normal but also good for us; it can enhance our ability to cope with stress by making cells more resilient. It also improves mental and physical performance and protects against aging and disease. Intermittent fasting is not the latest fad diet; it doesn’t dictate food choice or quantity. It doesn’t make money for the pharmaceutical, processed food, or health care industries. Intermittent fasting is an eating pattern that includes frequent periods of time with little or negligible amounts of food. It is often accompanied by weight loss, but, Mattson says, studies show that its remarkable beneficial effects cannot be accounted for by weight loss alone. Mattson—whose pioneering research uncovered the ways that the brain responds to fasting and exercise—explains how thriving while fasting became an evolutionary adaptation. He describes the specific ways that intermittent fasting slows aging; reduces the risk of diseases, including obesity, Alzheimer’s, and diabetes; and improves …

Introduction Transcranial Magnetic Stimulation (TMS) is a noninvasive technique that uses pulsed magnetic fields to affect the physiology of the brain and central nervous system. Repetitive TMS (rTMS) has been used to study and treat several neurological conditions, but its complex molecular basis is largely unexplored. Methods Utilizing three experimental rat models (in vitro, ex vivo, and in vivo) and employing genome-wide microarray analysis, our study reveals the extensive impact of rTMS treatment on gene expression patterns. Results These effects are observed across various stimulation protocols, in diverse tissues, and are influenced by time and age. Notably, rTMS-induced alterations in gene expression span a wide range of biological pathways, such as glutamatergic, GABAergic, and anti-inflammatory pathways, ion channels, myelination, mitochondrial energetics, multiple neuron-and synapse-specific genes. Discussion This comprehensive transcriptional analysis induced by rTMS stimulation serves as a foundational characterization for subsequent experimental investigations and the exploration of potential clinical applications.

Aging is the major risk factor for Alzheimer’s disease (AD). Mitochondrial dysfunction and neuronal network hyperexcitability are two age-related alterations implicated in AD pathogenesis. We found that levels of the mitochondrial protein deacetylase sirtuin-3 (SIRT3) are significantly reduced, and consequently mitochondria protein acetylation is increased in brain cells during aging. SIRT3-deficient mice exhibit robust mitochondrial protein hyperacetylation and reduced mitochondrial mass during aging. Moreover, SIRT3-deficient mice exhibit epileptiform and burst-firing electroencephalogram activity indicating neuronal network hyperexcitability. Both aging and SIRT3 deficiency result in increased sensitivity to kainic acid-induced seizures. Exposure of cultured cerebral cortical neurons to amyloid β-peptide (Aβ) results in a reduction in SIRT3 levels and SIRT3-deficient neurons exhibit heightened sensitivity to Aβ …