Photobiomodulation (PBM) describes the use of red or near-infrared light to stimulate, heal, regenerate, and protect tissue that has either been injured, is degenerating, or else is at risk of dying. One of the organ systems of the human body that is most necessary to life, and whose optimum functioning is most worried about by […]
Shining light on the head: Photobiomodulation for brain disorders Read More »
The intricate connection between central and enteric nervous systems is well established with emerging evidence linking gut microbiota function as a significant new contributor to gut-brain axis signaling. Several microbial signals contribute to altered gut-brain communications, with steroids representing an important biological class that impacts central and enteric nervous system function. Neuroactive steroids contribute pathologically
Gut Feelings: The Microbiota-Gut-Brain Axis on Steroids Read More »
The blood-brain barrier (BBB) is a fundamental component of the central nervous system(CNS). Its functional and structural integrity is vital to maintain the homeostasis of the brain microenvironment by controlling the passage of substances and regulating the trafficking of immune cellsbetween the blood and the brain. The BBB is primarily composed of highly specialized microvascular
The ability to detect oxygen availability is a ubiquitous attribute of aerobic organisms. However, the mechanism(s) that transduce oxygen concentration or availability into appropriate physiological responses is less clear and often controversial. This review will make the case for oxygen-dependent metabolism of hydrogen sulfide (H2S) and polysulfides, collectively referred to as reactive sulfur species (RSS)
A Case for Hydrogen Sulfide Metabolism as an Oxygen Sensing Mechanism Read More »
Objectives: The objective of this study was to introduce the evidence obtained throughextensive research that periodontitis increases risk of many systemic diseases. Method: Analysis of some oral bacteria (P. gingivalis, T. denticola, T. forsythia, A.actinomycetemcomitans, and F. nucleatum) and its related treatments and mediatorsby the specific methods (western blot, ELISA, etc). Results: This article reviews
The pathogenic mechanism of oral bacteria and treatment with inhibitors Read More »
Alpha-synuclein protein is associated with Parkinson’s disease and is an intrinsically disordered protein (IDP) in solution. The protein consists of three domains: N-terminal domain, NAC domain, and C-terminal domain. In this research, I used the Gaussian accelerated Molecular Dynamics (GaMD) simulations to examine the role of the flanking domains of the protein. My data show
PROTECTIVE ROLE OF THE FLANKING DOMAINS AND MEMBRANE SELECTIVITY IN THE ALPHA-SYNUCLEIN Read More »
Over the past decades, any attempt at identifying a single, curative treatment for neurodegenerative conditions has failed. For example, over 200 drugs for Alzheimer’s disease (AD) have all but come and gone without any significant contribution to better management of this devastating condition. Clearly this is not for the lack of effort or funding, but
The role of molecular chaperones, such as heat shock protein 70 (Hsp70), is not typically studied as a function of biological sex, but by addressing this gap we might improve our understanding of proteinopathic disorders that predominate in one sex. Therefore, we exposed male or female primary hippocampal cultures to preformed α-synuclein fibrils in a
Heat Shock Protein 70 as a Sex-Skewed Regulator of α-Synucleinopathy Read More »
This chapter contrasts the prion-like behavior of alphasynuclein in Parkinson’s disease with other prion diseases.In prion diseases, the infectious, amyloid form of theprotein induces the corresponding normally folded proteinto assume the toxic fold, spreading the disease and slowlydestroying the brains of infected patients. Lewy pathologyin Parkinson’s disease appears to spread in a mannersimilar to that
We identified 4 modifiers: aux, Lrrk, Ric, and Vps13, orthologs of the human genes GAK, LRRK2, RIT2, and VPS13C, respectively. Knockdown of each gene exacerbated neurodegeneration as measured by total and dopaminergic neuron loss. Knockdown of each modifier also increased α-synuclein oligomerization. These results suggest that some Parkinson’s disease risk genes exert their effects in glia and that glia can influence
Parkinson’s disease risk genes act in glia to control neuronal α-synuclein toxicity Read More »