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.

Nectandrin B significantly increases the lifespan of Drosophila - Nectandrin B for longevity.

Phytochemicals are increasingly recognized in the field of healthy aging as potential therapeutics against various aging-related diseases. Nutmeg, derived from the Myristica fragrans tree, is an example. Nutmeg has been extensively studied and proven to possess antioxidant properties that protect against aging and alleviate serious diseases such as cancer, heart disease, and liver disease. However, the specific active ingredient in nutmeg responsible for these health benefits has not been identified thus far. In this study, we present evidence that Nectandrin B (NecB), a bioactive lignan compound isolated from nutmeg, significantly extended the lifespan of the fruit fly Drosophila melanogaster by as much as 42.6% compared to the control group. NecB also improved age-related symptoms including locomotive deterioration, body weight gain, eye degeneration, and neurodegeneration in aging D. melanogaster. This result represents the most substantial improvement in lifespan observed in animal experiments to date, suggesting that NecB may hold promise as a potential therapeutic agent for promoting longevity and addressing age-related degeneration.

Oxidizability assay of unfractionated plasma of patients' with different plasma profile: a methodological study.

BACKGROUND: Present study describe the in vitro model of plasma oxidation of patients with different lipid profile, that can be correlated to their invivo plasma oxidizability in order to find the arterial diseases prone patient groups. METHOD: The method applied here to measure the invitro plasma oxidizability, accounts a convenient way that can be well suited in any clinical laboratory settings. Un-fractionated plasma was exposed to CuSO4 (5.0 mmol/L), a pro-oxidant, and low frequency ultrasonic wave to induce oxidation, and finally oxidizability was calculated by TBARS and Conjugated Diene methods. RESULT: In our study, plasma LDL greater than 150 mg/dL possess 1.75 times more risk to undergo oxidation (CI, 0.7774 to 3.94; p = 0.071) than the low LDL plasma, percent of oxidation increased from 38.3% to 67.1% for the LDL level upto 150 mg/dL and high. Lag phase, which is considered as the plasma antioxidative protection, was also influenced by the higher LDL concentration. The mean lag time was 65.27 ± 20.02 (p = 0.02 compared to healthy), where as for 94.71 ± 35.11 min for the normolipidemic subject. The plasma oxidizability was also changed drastically for total cholesterol level, oxidative susceptibility shown 35% and 55.02% for 200 mg/dL and high respectively, however it didn't appear as risk factor. Patient samples were also stratified according to their age, gender, and blood glucose level. Older persons (≥40 years) were 1.096 times (95% CL, 0.5607 to 2.141, p = 0.396) than younger (≤39 years age), males are 1.071 (95% CI, 0.5072- 2.264) times than the females, and diabetic patients are 1.091 (CI, 0.6153 to 1.934, p = 0.391) times in more risk than the non-diabetic counterpart. CONCLUSION: This method addressing its easy applicability in biomedical research. And by this we were able to show that patients with high LDL (≥150 mg/dL) are in alarming condition besides diabetic and elderly (≥40 years age) males are considered to be susceptible and more prone to develop vascular diseases.

Alpha amylase enzyme inhibitory and anti-inflammatory effect of Lawsonia inermis.

Previously it was reported elsewhere that Lawsonia inermis have anti-inflammatory and analgesic effect in experimental animals. The in vitro porcine alpha amylase inhibitory effect was investigated of this plant methanolic extracts and consequently hypoglycemic effect by quantitatively determining the maltose from the maltose standard curve while the anti-inflammatory effect by acetic acid induced writhing test in mice. Acarbose (10 microg mL(-1)) and Diclofenac sodium (20 mg kg(-1)) were used as reference hypoglycemic and anti-inflammatory drugs, respectively, for this study. The methanolic leaves extract of the plant significantly inhibited (60.97% compared to untreated) enzymatic activity of the amylase at 10 microg mL(-1) dose (p < 0.05) also reduced the chemically induced nociceptive pain stimuli significantly at all doses (p < 0.01). Carbohydrates, glycosides, flavonoids, saponins and tannins were found to have in phytochemical screening of the extract which are thought to bring these effects. For the conclusive purpose, it is suggesting from the result that the pharmacological properties of this Lawsonia inermis can elicit hypoglycemic effect by inhibiting alpha-amylase enzyme and can reduce neurogenic pain stimulus. It gives the notion that how this group of patient would be therapeutically benefitted by decreasing both these effects by the same agent which is easy available.