Review: The Prion and Its Potentiality

A great deal of effort during the past 27 years has been devoted to defining the chemical nature of prions, the infectious agents responsible for transmissible spongiform encephalopathies. Prion diseases are fatal neurodegenerative disorders that can arise spontaneously, be inherited, or be acquired by infection in mammals. They are unique not only in terms of their biological features but also in terms of their impact on public health. It has been hypothesized that in addition to Creutzfeldt - Jakob disease (CJD) in humans and Bovine Spongiform Encephalopathy (BSE) in animals, prions may also play a role in several other neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and frontotemporal dementia; however, the precise mechanism underlying prion-mediated neurodegeneration still remains elusive. In this review, we outline the physico-chemical characteristics of prions and their impact on human and animal health

Dysbiosis of the gut microbiota and its effect on α-synuclein and prion protein misfolding: consequences for neurodegeneration

Abnormal behavior of α-synuclein and prion proteins is the hallmark of Parkinson’s disease (PD) and prion illnesses, respectively, being complex neurological disorders. A primary cause of protein aggregation, brain injury, and cognitive loss in prion illnesses is the misfolding of normal cellular prion proteins (PrPC) into an infectious form (PrPSc). Aggregation of α-synuclein causes disruptions in cellular processes in Parkinson’s disease (PD), leading to loss of dopamine-producing neurons and motor symptoms. Alteration in the composition or activity of gut microbes may weaken the intestinal barrier and make it possible for prions to go from the gut to the brain. The gut-brain axis is linked to neuroinflammation; the metabolites produced by the gut microbiota affect the aggregation of α-synuclein, regulate inflammation and immunological responses, and may influence the course of the disease and neurotoxicity of proteins, even if their primary targets are distinct proteins. This thorough analysis explores the complex interactions that exist between the gut microbiota and neurodegenerative illnesses, particularly Parkinson’s disease (PD) and prion disorders. The involvement of the gut microbiota, a complex collection of bacteria, archaea, fungi, viruses etc., in various neurological illnesses is becoming increasingly recognized. The gut microbiome influences neuroinflammation, neurotransmitter synthesis, mitochondrial function, and intestinal barrier integrity through the gut-brain axis, which contributes to the development and progression of disease. The review delves into the molecular mechanisms that underlie these relationships, emphasizing the effects of microbial metabolites such as bacterial lipopolysaccharides (LPS), and short-chain fatty acids (SCFAs) in regulating brain functioning. Additionally, it looks at how environmental influences and dietary decisions affect the gut microbiome and whether they could be risk factors for neurodegenerative illnesses. This study concludes by highlighting the critical role that the gut microbiota plays in the development of Parkinson’s disease (PD) and prion disease. It also provides a promising direction for future research and possible treatment approaches. People afflicted by these difficult ailments may find hope in new preventive and therapeutic approaches if the role of the gut microbiota in these diseases is better understood

Hong_Microarray Dataset

The compositional variation of the Formula Diet fed to the experimental mice (Additional table file), Differentially expressed genes by effect of RS, DJ, and DJ526 (Additional table file), The most highly significant up-regulated and down-regulated pathways in the livers of mice on RS, DJ and DJ526 towards those on Ctrl groups (Additional table file), Globally normalized data (Fold change raw data file), Z transformed data (Z-ratio raw data file), and GSEA results (GSEA results data file

Hong_Figshare 1.zip

The compositional variation of the Formula Diet fed to the experimental mice (Additional table file), Differentially expressed genes by effect of RS, DJ, and DJ526 (Additional table file), The most highly significant up-regulated and down-regulated pathways in the livers of mice on RS, DJ and DJ526 towards those on Ctrl groups (Additional table file), Globally normalized data (Fold change raw data file), Z transformed data (Z-ratio raw data file), and GSEA results (GSEA results data file

The gene expression profile and physiological data of mice feeding the resveratrol-enriched rice DJ526

The raw data for the blood serum analyses on mice fed with resveratrol (RS), Dongjin rice (DJ), and the resveratrol-enriched rice DJ526 (DJ526), the raw data for mouse behavioral tests of RS, DJ, and DJ526 groups, the raw data for qRT-PCR results of the livers of the mice of RS, DJ and DJ526 groups compared with Ctrl groups, Globally normalized data (Fold change raw data file), Z transformed data (Z-ratio raw data file), and ARRIVE guidelines Checklis

The gene expression profile of mice feeding the resveratrol-enriched rice DJ526

The blood assay measurements raw data by effect of RS, DJ, and DJ526 (Additional data file), unprocessed behavioral raw data by effect of RS, DJ, and DJ526 (Additional data file), the measurement-level qRT-PCR raw data in the livers of mice on RS, DJ and DJ526 towards those on Ctrl groups (Additional data file), Globally normalized data (Fold change raw data file), Z transformed data (Z-ratio raw data file), and GSEA results (GSEA results data file