https://pubmed.ncbi.nlm.nih.gov/33951489/

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https://www.nature.com/articles/d41586-024-00169-7.pdf

Leonardo Trasande, Roopa Krithivasan, Kevin Park, Vladislav Obsekov, Michael Belliveau, Chemicals Used in Plastic Materials: An Estimate of the Attributable Disease Burden and Costs in the United States, Journal of the Endocrine Society, Volume 8, Issue 2, February 2024, bvad163, https://doi.org/10.1210/jendso/bvad163

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Exposure to endocrine-disrupting chemicals (EDCs) via daily use of plastics is a major contributor to the overall disease burden in the United States and the associated costs to society amount to more than 1% of the gross domestic product, revealed a large-scale analysis.

The research, published in the Journal of the Endocrine Society on January 11, indicated that taken together, the disease burden attributable to EDCs used in the manufacture of plastics added up to almost $250 billion in 2018 alone.

https://www.medscape.com/viewarticle/whats-disease-burden-plastic-exposure-2024a10000q4

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Report on Microplastics in Hong Kong:

Vogt N. Predicting neural activity from facial expressions. Nat Methods. 2024 Jan;21(1):9. doi: 10.1038/s41592-023-02154-w. PMID: 38212550.

https://pubmed.ncbi.nlm.nih.gov/38212550/

https://www.nature.com/articles/s41593-023-01490-6.pdf

https://www.cityu.edu.hk/sds/web/pesports_healthyu_EIM_Series.shtml

Background: Physical activity (PA) represents a promising behavioral approach for managing cognitive dysfunction in multiple sclerosis (MS). However, there is a lack of information on the pattern of free-living PA intensity (e.g., step rate) and its unique association with cognition. Such information is essential for informing clinical trials in MS.

Objective: We examined associations among PA volume and intensity with cognitive function in persons with MS, and intensity was derived from steps-based metrics (peak 30-min cadence [Peak-30_CAD], and time spent in incremental cadence bands).

Methods: We included data from 147 persons with MS who underwent assessments of cognitive function (via Brief International Cognitive Assessment in MS) and wore an ActiGraph GT3X + accelerometer for 7 days. We performed bivariate and partial correlations and regression analyses examining associations among PA metrics and cognitive outcomes.

Results: Higher Peak-30_CAD was significantly associated with better performance in cognitive processing speed and verbal learning and memory (r_s = 0.19-0.38), and the associations remained significant when controlling for daily steps, age, sex, and years of education (p < 0.05). By comparison, daily steps was only correlated with cognitive processing speed (r_s = 0.26), and the association was non-significant when controlling for Peak-30_CAD and covariates. There were stronger correlations among time spent in higher intensity cadence bands with cognitive performance (r_s = 0.18-0.38).

Conclusion: Our results highlight the important role of PA intensity for cognition in MS, and may inform future development of focal PA interventions that focusing on step rate patterns for improving cognition in persons with MS.

Zheng P, Sandroff BM, Motl RW. Free-living ambulatory physical activity and cognitive function in multiple sclerosis: the significance of step rate vs. step volume. J Neurol. 2024 Jan 12. doi: 10.1007/s00415-023-12169-0. Epub ahead of print. PMID: 38214757.

https://pubmed.ncbi.nlm.nih.gov/38214757/

Abstract:  Essential metals play critical roles in maintaining human health as they participate in various physiological activities. Nonetheless, both excessive accumulation and deficiency of these metals may result in neurotoxicity secondary to neuroinflammation and the activation of microglia and astrocytes. Activation of these cells can promote the release of pro-inflammatory cytokines. It is well known that neuroinflammation plays a critical role in metal-induced neurotoxicity as well as the development of neurological disorders, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Initially seen as a defense mechanism, persistent inflammatory responses are now considered harmful. Astrocytes and microglia are key regulators of neuroinflammation in the central nervous system, and their excessive activation may induce sustained neuroinflammation. Therefore, in this review, we aim to emphasize the important role and molecular mechanisms underlying metal-induced neurotoxicity. Our objective is to raise the awareness on metal-induced neuroinflammation in neurological disorders. However, it is not only just neuroinflammation that different metals could induce; they can also cause harm to the nervous system through oxidative stress, apoptosis, and autophagy, to name a few. The primary pathophysiological mechanism by which these metals induce neurological disorders remains to be determined. In addition, given the various pathways through which individuals are exposed to metals, it is necessary to also consider the effects of co-exposure to multiple metals on neurological disorders.

Wei R, Wei P, Yuan H, Yi X, Aschner M, Jiang YM, Li SJ. Inflammation in Metal-Induced Neurological Disorders and Neurodegenerative Diseases. Biol Trace Elem Res. 2024 Jan 11. doi: 10.1007/s12011-023-04041-z. Epub ahead of print. PMID: 38206494.

https://pubmed.ncbi.nlm.nih.gov/38206494/

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Tissue Response to Neural Implants: The Use of Model Systems Toward New Design Solutions of Implantable Microelectrodes

Abstract:  “The development of implantable neuroelectrodes is advancing rapidly as these tools are becoming increasingly ubiquitous in clinical practice, especially for the treatment of traumatic and neurodegenerative disorders. Electrodes have been exploited in a wide number of neural interface devices, such as deep brain stimulation, which is one of the most successful therapies with proven efficacy in the treatment of diseases like Parkinson or epilepsy. However, one of the main caveats related to the clinical application of electrodes is the nervous tissue response at the injury site, characterized by a cascade of inflammatory events, which culminate in chronic inflammation, and, in turn, result in the failure of the implant over extended periods of time…”

Gulino M, Kim D, Pané S, Santos SD, Pêgo AP. Tissue Response to Neural Implants: The Use of Model Systems Toward New Design Solutions of Implantable Microelectrodes. Front Neurosci. 2019 Jul 5;13:689. doi: 10.3389/fnins.2019.00689. PMID: 31333407; PMCID: PMC6624471.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6624471/

Abstract:  Alzheimer’s disease (AD) has characteristic histopathological, molecular, and biochemical abnormalities, including cell loss; abundant neurofibrillary tangles; dystrophic neurites; amyloid precursor protein, amyloid-β (APP-Aβ) deposits; increased activation of prodeath genes and signaling pathways; impaired energy metabolism; mitochondrial dysfunction; chronic oxidative stress; and DNA damage. Gaining a better understanding of AD pathogenesis will require a framework that mechanistically interlinks all these phenomena. Currently, there is a rapid growth in the literature pointing toward insulin deficiency and insulin resistance as mediators of AD-type neurodegeneration, but this surge of new information is riddled with conflicting and unresolved concepts regarding the potential contributions of type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity to AD pathogenesis. Herein, we review the evidence that (1) T2DM causes brain insulin resistance, oxidative stress, and cognitive impairment, but its aggregate effects fall far short of mimicking AD; (2) extensive disturbances in brain insulin and insulin-like growth factor (IGF) signaling mechanisms represent early and progressive abnormalities and could account for the majority of molecular, biochemical, and histopathological lesions in AD; (3) experimental brain diabetes produced by intracerebral administration of streptozotocin shares many features with AD, including cognitive impairment and disturbances in acetylcholine homeostasis; and (4) experimental brain diabetes is treatable with insulin sensitizer agents, i.e., drugs currently used to treat T2DM. We conclude that the term “type 3 diabetes” accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both type 1 diabetes mellitus and T2DM.

de la Monte SM, Wands JR. Alzheimer’s disease is type 3 diabetes-evidence reviewed. J Diabetes Sci Technol. 2008 Nov;2(6):1101-13. doi: 10.1177/193229680800200619. PMID: 19885299; PMCID: PMC2769828.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/

DOI:https://doi.org/10.1016/j.stemcr.2023.10.003

Abstract:  The advancement in epigenetics research over the past several decades has led to the potential application of epigenome-editing technologies for the treatment of various diseases. In particular, epigenome editing is potentially useful in the treatment of genetic and other related diseases, including rare imprinted diseases, as it can regulate the expression of the epigenome of the target region, and thereby the causative gene, with minimal or no modification of the genomic DNA. Various efforts are underway to successfully apply epigenome editing in vivo, such as improving target specificity, enzymatic activity, and drug delivery for the development of reliable therapeutics. In this review, we introduce the latest findings, summarize the current limitations and future challenges in the practical application of epigenome editing for disease therapy, and introduce important factors to consider, such as chromatin plasticity, for a more effective epigenome editing-based therapy.

Ueda J, Yamazaki T, Funakoshi H. Toward the Development of Epigenome Editing-Based Therapeutics: Potentials and Challenges. Int J Mol Sci. 2023 Mar 1;24(5):4778. doi: 10.3390/ijms24054778. PMID: 36902207; PMCID: PMC10003136.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10003136/