Prevention Of Neurodegenerative Diseases Research Articles

From ice to neurons: investigating the neuroprotective effects of Antarctic microalgae Chlorella variabilis and Chlorella pyrenoidosa extracts.

In this study, it was aimed to examine the neuroprotective effects of ethanolic extracts of Chlorella variabilis YTU.ANTARCTIC.001and Chlorella pyrenoidosa OZCIMEN.001microalgae that were isolated from Antarctica in a H2O2-induced oxidative stress model using SH-SY5Y cell line. In this context, first, Antarctic microalgae were cultivated and characterized. It was determined that C. pyrenoidosa and C. variabilis had specific growth rates of 0.093 and 0.097day-1, respectively, and doubled their cell concentration in 7days. With the antioxidant and phenolic content analysis, it was found that 1mg/mL C. pyrenoidosa and C. variabilis ethanolic extracts had 33-37% radical scavenging activity and 102-107mg GAE/mg extract phenolic content, respectively. Then, the cytotoxic effects of the microalgae extracts on SH-SY5Y cells were assessed across a concentration range of 6.25-125µg/mL. The results indicated a concentration-dependent effect on cell viability, with no observed cytotoxicity within the tested range. Notably, the highest neuroprotective activity was recorded with C. variabilisextract at a concentration of 75µg/mL, which maintained cell viability at 73.7% ± 0.3. These findings showed the significant neuroprotective potential of C. pyrenoidosaandC. variabilisethanolic extracts, attributed to their substantial antioxidant properties and non-cytotoxic nature at effective concentrations. The promising neuroprotective efficacy of these extracts highlights their potential for therapeutic applications in neurodegenerative disease prevention and treatment.

Unveiling the link between glymphatic function and cortical microstructures in post-traumatic stress disorder

PurposeThe discovery of the glymphatic system, crucial for cerebrospinal and interstitial fluid exchange, has enhanced our grasp of brain protein balance and its potential role in neurodegenerative disease prevention and therapy. Detecting early neurodegenerative shifts via noninvasive biomarkers could be key in identifying at-risk individuals for Alzheimer's disease (AD). Our research explores a diffusion tensor imaging (DTI) method that measures cortical mean diffusivity (cMD), potentially a more sensitive indicator of neurodegeneration than traditional macrostructural methods. Materials and methodsWe analyzed 67 post-traumatic stress disorder (PTSD)-diagnosed veterans from the Alzheimer's Disease Neuroimaging Initiative database. Participants underwent structural MRI, DTI, Aβ PET imaging, and cognitive testing. We focused on the DTI-ALPS technique to assess glymphatic function and its relation to cMD, cortical Aβ accumulation, and thickness, accounting for age and APOE ε4 allele variations. ResultsThe cohort, all male with an average age of 68.1 (SD 3.4), showed a strong inverse correlation between DTI-ALPS and cMD in AD-affected regions, especially in the entorhinal, parahippocampal, and fusiform areas. Higher DTI-ALPS readings were consistently linked with greater cortical thickness, independent of Aβ deposits and genetic risk factors. Age and cMD emerged as inversely proportional predictors of DTI-ALPS, indicating a complex interaction with age. ConclusionThe study confirms a meaningful association between glymphatic efficiency and cMD in AD-sensitive zones, accentuating cortical microstructural alterations in PTSD. It positions DTI-ALPS as a viable biomarker for assessing glymphatic function in PTSD, implicating changes in DTI-ALPS as indicative of glymphatic impairment.

Impact of Helicobacter pylori eradication on age-specific risk of incident dementia in patients with peptic ulcer disease: a nationwide population-based cohort study.

The impact of peptic ulcer disease (PUD) and Helicobacter pylori (H. pylori) eradication therapy on dementia risk in high H. pylori prevalence populations remains uncertain. This study investigates the relationship between PUD, H. pylori eradication, and dementia risk, including Alzheimer's disease (AD), in an elderly South Korean cohort, considering age and eradication timing. Data from the Korean National Health Insurance Service (2002-2015) for individuals aged 55-79 were analyzed. Participants were divided based on PUD and H. pylori therapy status. Propensity score matching was used to evaluate dementia incidence and hazard ratios over 5 and 10 years, alongside the timing of eradication therapy. PUD is linked to higher dementia risk at 5 and 10 years, more for overall dementia than AD, with eradication status not significantly altering the risk. Age-specific analysis showed increased AD risk in the 60s and 70s age groups. Late eradication therapy is correlated with a higher dementia risk. PUD is a risk factor for dementia in elderly South Koreans, particularly with delayed H. pylori therapy. The findings emphasize timely H. pylori management and its potential role in neurodegenerative disease prevention.

Effect of polycyclic aromatic hydrocarbon exposure on amnestic mild cognitive impairment and Alzheimer’s disease: A matched case-control study

There is an emerging body of evidence concerning the neurological effect of air pollutants on cognitive function and increased risk of neurodegeneration. Although previous studies have suggested that polycyclic aromatic hydrocarbons (PAHs) are neurotoxic, the effect of PAHs exposure on neurodegeneration remains unclear. This study aimed to investigate the association between PAH exposure and the risk of developing amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD). For this matched case-control cross-sectional study, we recruited patients aged ≥50 years diagnosed with aMCI and AD from the Samsung Medical Center, Seoul, Korea, between 2014 and 2019. For each patient, we randomly selected four cognitively healthy controls through frequency matching based on sex, age group, and education level. Urinary levels of four PAH metabolites, 1-hydroxypyrene (1-OHP), 1-hydroxyphenanthrene (1-OHPhe), 2-hydroxyfluorene (2-OHFlu), and 2-naphthol (2-NAP), were measured. A conditional logistic regression model was used to evaluate the association, adjusting for potential confounders. A total of 212 patients with aMCI with 848 matched controls, and 267 patients with AD with 1068 matched controls were included in the analyses to estimate the risk of PAH exposure. We found that elevated urinary levels of PAH metabolites (specifically, 1-OHP and 2-NAP) were significantly associated with an increased risk of aMCI and AD. An increase of one unit in log-transformed level of urinary 1-OHP was associated with a 1.15- and 1.16-times higher risk of aMCI and AD, respectively. An increase of one unit in log-transformed level of urinary 2-NAP was associated with a 1.11- and 1.13-times higher risk of aMCI and AD, respectively. These findings indicate that PAH exposure may increase the risk of aMCI and AD, especially for the elderly population. Considering the widespread distribution of PAHs in the environment, reducing PAH exposure may be an effective strategy for the prevention of neurodegenerative diseases.

Neuroprotective Effects of Olive Oil: A Comprehensive Review of Antioxidant Properties.

Neurodegenerative diseases are a significant challenge to global healthcare, and oxidative stress plays a crucial role in their development. This paper presents a comprehensive analysis of the neuroprotective potential of olive oil, with a primary focus on its antioxidant properties. The chemical composition of olive oil, including key antioxidants, such as oleuropein, hydroxytyrosol, and oleocanthal, is systematically examined. The mechanisms by which these compounds provide neuroprotection, including counteracting oxidative damage and modulating neuroprotective pathways, are explored. The neuroprotective efficacy of olive oil is evaluated by synthesizing findings from various sources, including in vitro studies, animal models, and clinical trials. The integration of olive oil into dietary patterns, particularly its role in the Mediterranean diet, and its broader implications in neurodegenerative disease prevention are also discussed. The challenges in translating preclinical findings to clinical applications are acknowledged and future research directions are proposed to better understand the potential of olive oil in mitigating the risk of neurodegenerative conditions. This review highlights olive oil not only as a dietary component, but also as a promising candidate in preventive neurology, advocating for further investigation in the context of neurodegenerative diseases.

Effectiveness of Flavonoid-Rich Diet in Alleviating Symptoms of Neurodegenerative Diseases.

Over the past decades, there has been a significant increase in the burden of neurological diseases, including neurodegenerative disorders, on a global scale. This is linked to a widespread demographic trend in which developed societies are aging, leading to an increased proportion of elderly individuals and, concurrently, an increase in the number of those afflicted, posing one of the main public health challenges for the coming decades. The complex pathomechanisms of neurodegenerative diseases and resulting varied symptoms, which differ depending on the disease, environment, and lifestyle of the patients, make searching for therapies for this group of disorders a formidable challenge. Currently, most neurodegenerative diseases are considered incurable. An important aspect in the fight against and prevention of neurodegenerative diseases may be broadly understood lifestyle choices, and more specifically, what we will focus on in this review, a diet. One proposal that may help in the fight against the spread of neurodegenerative diseases is a diet rich in flavonoids. Flavonoids are compounds widely found in products considered healthy, such as fruits, vegetables, and herbs. Many studies indicated not only the neuroprotective effects of these compounds but also their ability to reverse changes occurring during the progression of diseases such as Alzheimer's, Parkinson's and amyotrophic lateral sclerosis. Here, we present the main groups of flavonoids, discussing their characteristics and mechanisms of action. The most widely described mechanisms point to neuroprotective functions due to strong antioxidant and anti-inflammatory effects, accompanied with their ability to penetrate the blood-brain barrier, as well as the ability to inhibit the formation of protein aggregates. The latter feature, together with promoting removal of the aggregates is especially important in neurodegenerative diseases. We discuss a therapeutic potential of selected flavonoids in the fight against neurodegenerative diseases, based on in vitro studies, and their impact when included in the diet of animals (laboratory research) and humans (population studies). Thus, this review summarizes flavonoids' actions and impacts on neurodegenerative diseases. Therapeutic use of these compounds in the future is potentially possible but depends on overcoming key challenges such as low bioavailability, determining the therapeutic dose, and defining what a flavonoid-rich diet is and determining its potential negative effects. This review also suggests further research directions to address these challenges.

Accurate identification of individuals with subjective cognitive decline using 3D regional fractal dimensions on structural magnetic resonance imaging

Background and ObjectiveAccurate identification of individuals with subjective cognitive decline (SCD) is crucial for early intervention and prevention of neurodegenerative diseases. Fractal dimensionality (FD) has emerged as a robust and replicable measure, surpassing traditional geometric metrics, in characterizing the intricate fractal geometrical properties of brain structure. Nevertheless, the effectiveness of FD in identifying individuals with SCD remains largely unclear. A 3D regional FD method can be suggested to characterize and quantify the spatial complexity of the precise gray matter, providing insights into cognitive aging and aiding in the automated identification of individuals with SCD. MethodsThis study introduces a novel integer ratio based 3D box-counting fractal analysis (IRBCFA) to quantify regional fractal dimensions (FDs) in structural magnetic resonance imaging (MRI) data. The innovative method overcomes limitations of conventional box-counting techniques by accommodating arbitrary box sizes, thereby enhancing the precision of FD estimation in small, yet neurologically significant, brain regions. ResultsThe application of IRBCFA to two publicly available datasets, OASIS-3 and ADNI, consisting of 520 and 180 subjects, respectively. The method identified discriminative regions of interest (ROIs) predominantly within the limbic system, fronto-parietal region, occipito-temporal region, and basal ganglia-thalamus region. These ROIs exhibited significant correlations with cognitive functions, including executive functioning, memory, social cognition, and sensory perception, suggesting their potential as neuroimaging markers for SCD. The identification model trained on these ROIs demonstrated exceptional performance achieving over 93 % accuracy on the discovery dataset and exceeding 87 % on the independent testing dataset. Furthermore, an exchange experiment between datasets revealed a substantial overlap in discriminative ROIs, highlighting the robustness of our method across diverse populations. ConclusionOur findings indicate that IRBCFA can serve as a valuable tool for quantifying the spatial complexity of gray matter, providing insights into cognitive aging and aiding in the automated identification of individuals with SCD. The demonstrated generalizability and robustness of this method position it as a promising tool for neurodegenerative disease research and offer potential for clinical applications.

Entertainment activities and the risk of Alzheimer's disease: a Mendelian randomization analysis.

Effective prevention is key to addressing the increasing prevalence and mortality of Alzheimer's disease. Assessing the causal relationship between modifiable entertainment activity factors and the risk of Alzheimer's disease is important for developing public health measures, but establishing causal relationships in epidemiological data may be challenging. This study using the two-sample Mendelian randomization analysis aimed to investigate the causal effect of entertainment activity factors on the risk of Alzheimer's disease. Summary statistics from publicly available genome-wide association studies were used to analyze 14 modifiable entertainment activity. The inverse variance weighted random effects method as the primary analytical method to estimate causal effects was used. Additionally performed MR-Egger, weighted median and weighted model methods to assess the robustness of the results. The reliability of our findings was validated through systematic sensitivity analyses and tests for heterogeneity. We found significant correlation between time spent using computer (odds ratio 0.998; 95% confidence interval 0.996-0.999; p = 0.013) and Alzheimer's disease, compared to other studied entertainment activities that had no significant causal relationship with Alzheimer's disease. Our findings support the hypothesis that increased computer use may reduce the risk of Alzheimer's disease, providing potential strategic directions for the prevention of neurodegenerative diseases.

The role of CRMP4 in LPS-induced neuroinflammation

Neuroinflammation has been gaining attention as one of the potential causes of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis in recent years. The suppression of excessive proinflammatory responses is expected to be a target for the treatment and prevention of neurodegenerative diseases. Collapsin response mediator protein 4 (CRMP4) is involved in cytoskeleton-associated axonal guidance in the developing brain. Recently, the involvement of CRMP4 in several pathological conditions, including inflammation induced by lipopolysaccharide (LPS), a widely used inflammatory molecule, has been reported. However, the role of CRMP4 in LPS-induced inflammation in vivo remains largely unknown.In this study, we generated microglia-specific CRMP4 knockout mice for the first time and examined the role of CRMP4 in an LPS-induced brain inflammation model. We found that microglia after LPS injection in substantia nigra was significantly reduced in Crmp4-/- mice compared to Crmp4+/+mice. The increased expression of IL-10 in striatum samples was downregulated in Crmp4-/- mice. A significant reduction in Iba1 expression was also observed in microglia-specific Crmp4 knockout mice compared with that in control mice. In contrast, the expression of IL-10 did not change in these mice, whereas arginase 1 (Arg1) expression was significantly suppressed. These results demonstrate the involvement of CRMP4 in LPS-induced inflammation in vivo, that CRMP4 suppresses microglial proliferation in a cell-autonomous manner.

Modeling Neurodegeneration and Regeneration in Parkinson's Disease

The diagnosis and prevention of neurodegenerative diseases is a heavily examined topic in the neuroscience discipline. Whether it be from the anatomical and biological perspectives or the psychological and sociological perspectives, the ultimate goal is to discover strategies to pinpoint the infection as soon as possible. This article begins with reviewing the small-world network structure and then combines the sociological and anatomical perspectives to explain the progression of neuronal death within the brain by using rsfMRI data and the Hegselmann-Krause Model of Opinion Dynamics to illustrate critical interactions between brain regions, and to predict the ultimate behavior of the neural network after initial degeneration Following experimentation–in which critical regions related to Parkinson’s Disease were studied–thresholds were identified in specific regions which exhibited consistent converging behavior of the neural network toward either degenerative or regenerative directions. Furthermore, a simple graphical model is proposed to demonstrate the ranges of values in which current brain health could be of concern. We concluded that neuron death in one brain region can lead to further infection in the resulting system; however, some regions can also directly/indirectly compensate for the system’s decreased function. In future research endeavors, this could provide insight into developing more accurate predictive models for the goal of early detection of a diseased brain and its recovery.

The therapeutic potential of probucol and probucol analogues in neurodegenerative diseases.

Neurodegenerative disorders present complex pathologies characterized by various interconnected factors, including the aggregation of misfolded proteins, oxidative stress, neuroinflammation and compromised blood-brain barrier (BBB) integrity. Addressing such multifaceted pathways necessitates the development of multi-target therapeutic strategies. Emerging research indicates that probucol, a historic lipid-lowering medication, offers substantial potential in the realm of neurodegenerative disease prevention and treatment. Preclinical investigations have unveiled multifaceted cellular effects of probucol, showcasing its remarkable antioxidative and anti-inflammatory properties, its ability to fortify the BBB and its direct influence on neural preservation and adaptability. These diverse effects collectively translate into enhancements in both motor and cognitive functions. This review provides a comprehensive overview of recent findings highlighting the efficacy of probucol and probucol-related compounds in the context of various neurodegenerative conditions, including Alzheimer's disease, Parkinson's disease, Huntington's disease, and cognitive impairment associated with diabetes.

Green and shape-tunable synthesis of ellagic acid crystalline particles by tannic acid for neuroprotection against oxidative stress.

Oxidative stress (OS) plays an important role in the emergence and prevention of neurodegenerative diseases, such as Alzheimer's disease (AD). Excess reactive oxygen species (ROS) accumulated in a neuronal cell can lead to OS, producing cell injury and death. Seeking nanoantioxidants against AD-related oxidative stress has attracted a lot of attention, especially those potential antioxidant agents derived from natural polyphenols. However, the transformation of abundant plant polyphenols to antioxidative biomaterials against OS is still challenging. In this work, we report a new method to transform amorphous tannic acid (TA) into tailorable shaped ellagic acid (EA) crystalline particles without using an organic solvent. EA crystalline particles were generated from TA, which underwent a chemical transformation, in situ metal phenolic coordination and acid-induced assembly process, and the size and shape could be controlled by varying the amount of acid. As-prepared EA crystalline particles showed excellent stability in water and lysosomal mimicking fluid and possess unique fluorescence properties and a strong response in mass spectrometry, which is beneficial for their imaging analysis in cells and tissues. More importantly, EA particles have shown significant H2O2-related ROS scavenging ability, a high cellular uptake capacity, an excellent neuroprotective effect in PC12 cells, a high drug loading capacity and BBB permeability to enter the brain. Our study suggested that the EA crystalline particles show great potential for OS-mediated AD treatment.

Characterization and Exploration of the Neuroprotective Potential of Oat-Protein-Derived Peptides in PC12 Cells and Scopolamine-Treated Zebrafish.

Neurodegenerative disorders pose a substantial risk to human health, and oxidative stress, cholinergic dysfunction, and inflammation are the major contributors. The purpose of this study was to explore the neuroprotective effects of oat protein hydrolysate (OPH) and identify peptides with neuroprotective potential. This study is the first to isolate and identify OPH peptides with neuroprotective potential, including DFVADHPFLF (DF-10), HGQNFPIL (HL-8), and RDFPITWPW (RW-9), by screening via peptidomes and molecular-docking simulations. These peptides showed positive effects on the activity of antioxidant enzymes and thus reduced oxidative stress through regulation of Nrf2-keap1/HO-1 gene expression in vitro and in vivo. The peptides also significantly ameliorated scopolamine-induced cognitive impairment in the zebrafish model. This improvement was correlated with mitigation of MDA levels, AChE activity, and levels of inflammatory cytokines in the brains of zebrafish. Furthermore, these peptides significantly upregulated the mRNA expression of Bdnf, Nrf2, and Erg1 in the brains of zebrafish with neurodegenerative disorders. Collectively, oat peptides have potential for use as active components in nutraceutical applications for the prevention of neurodegenerative diseases.

Role of sleep in neurodegeneration: the consensus report of the 5th Think Tank World Sleep Forum.

Sleep abnormalities may represent an independent risk factor for neurodegeneration. An international expert group convened in 2021 to discuss the state-of-the-science in this domain. The present article summarizes the presentations and discussions concerning the importance of a strategy for studying sleep- and circadian-related interventions for early detection and prevention of neurodegenerative diseases. An international expert group considered the current state of knowledge based on the most relevant publications in the previous 5years; discussed the current challenges in the field of relationships among sleep, sleep disorders, and neurodegeneration; and identified future priorities. Sleep efficiency and slow wave activity during non-rapid eye movement (NREM) sleep are decreased in cognitively normal middle-aged and older adults with Alzheimer's disease (AD) pathology. Sleep deprivation increases amyloid-β (Aβ) concentrations in the interstitial fluid of experimental animal models and in cerebrospinal fluid in humans, while increased sleep decreases Aβ. Obstructive sleep apnea (OSA) is a risk factor for dementia. Studies indicate that positive airway pressure (PAP) treatment should be started in patients with mild cognitive impairment or AD and comorbid OSA. Identification of other measures of nocturnal hypoxia and sleep fragmentation could better clarify the role of OSA as a risk factor for neurodegeneration. Concerning REM sleep behavior disorder (RBD), it will be crucial to identify the subset of RBD patients who will convert to a specific neurodegenerative disorder. Circadian sleep-wake rhythm disorders (CSWRD) are strong predictors of caregiver stress and institutionalization, but the absence of recommendations or consensus statements must be considered. Future priorities include to develop and validate existing and novel comprehensive assessments of CSWRD in patients with/at risk for dementia. Strategies for studying sleep-circadian-related interventions for early detection/prevention of neurodegenerative diseases are required. CSWRD evaluation may help to identify additional biomarkers for phenotyping and personalizing treatment of neurodegeneration.

Sex, gender, and the prevention of neurodegenerative diseases

Sex, gender, and the prevention of neurodegenerative diseases

In Vitro Analysis of Selected Antioxidant and Biological Properties of the Extract from Large-Fruited Cranberry Fruits

This study investigated the in vitro antioxidant and biological properties of ethanol extracts obtained from the fruits of the highbush cranberry. The produced extracts exhibited a high content of polyphenols (1041.9 mg 100 g d.m.−1) and a high antioxidant activity (2271.2 mg TE g 100 d.m.−1 using the DPPH method, 1781.5 mg TE g 100 d.m.−1 using the ABTS method), as well as a substantial amount of vitamin C (418.2 mg 100 g d.m.−1). These extracts also demonstrated significant in vitro biological activity. Studies conducted on the Saccharomyces cerevisiae cellular model revealed the strong antioxidant effects of the extract, attributed to a significant reduction in the levels of reactive oxygen species (ROS) within the cells, confirming the utility of the extracts in mitigating oxidative stress. Moreover, inhibitory properties were demonstrated against factors activating metabolic processes characteristic of inflammatory conditions. It was observed that the cranberry extract inhibits the activity of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) non-selectively. Additionally, the extract was found to be a highly active inhibitor of acetylcholinesterase (AChE), potentially suggesting the applicability of this extract in the prevention of neurodegenerative diseases, including Alzheimer’s disease.

Untargeted metabolomics reveal pathways associated with neuroprotective effect of oxyresveratrol in SH-SY5Y cells

Oxyresveratrol has been documented benefits for neurodegenerative disease. However, the specific molecular mechanisms and pathways involved is currently limited. This study aimed to investigate the potential neuroprotective mechanisms of oxyresveratrol using rotenone-induced human neuroblastoma SH-SY5Y cytotoxicity. Cells were divided into the following groups: control, rotenone, and oxyresveratrol pre-treated before being exposed to rotenone. Cellular assays were performed to investigate neuroprotective effects of oxyresveratrol. The results showed that 20 μM oxyresveratrol was effective in preventing rotenone-induced cell death and decreasing ROS levels in the cells. The alteration of metabolites and pathways involved in the neuroprotective activities of oxyresveratrol were further investigated using LC-QTOF-MS/MS untargeted metabolomics approach. We hypothesized that oxyresveratrol's neuroprotective effects would be associated with neurodegenerative pathways. A total of 294 metabolites were identified. 7,8-dihydrobiopterin exhibited the highest VIP scores (VIP > 3.0; p < 0.05), thus considered a biomarker in this study. Our results demonstrated that pretreatment with oxyresveratrol upregulated the level of 7,8-dihydrobiopterin compared to the positive control. Pathway analysis verified that 7,8-dihydrobiopterin was primarily associated with phenylalanine, tyrosine, and tryptophan metabolism (impact = 1, p < 0.001), serving as essential cofactors for enzymatic function in the dopamine biosynthesis pathway. In conclusion, oxyresveratrol may be benefit for the prevention of neurodegenerative diseases by increasing 7,8-dihydrobiopterin concentration.

Effect of Andrographis paniculata Extracts on Regeneration and Prevention of Oxidative Stress Damage in Planaria

ABSTRACT This study explored the potential of Andrographis paniculata in regulating redox imbalance using planaria as a model organism. Decapitated planaria were regenerated in water, A. paniculata extract, hydrogen peroxide, and a combination of hydrogen peroxide and A. paniculata. The growth was 26% higher, locomotion 15% higher, and protein 35% higher in A. paniculata group. The stressed group had 33% higher growth, 17% higher locomotion, and 36% higher protein when treated with A. paniculata. In conclusion, A. paniculata accelerated the regeneration and minimized the stress induced by hydrogen peroxide and hence can be a promising option for the prevention of neurodegenerative diseases.

Brain and Lifespan Science Homo sapiens: Energy, Quantum, Biophysical, Biochemical and Chronobiological Loss of Controllability Cognitive Brains of Healthy Aging Processes

Cognitive brain science is a new, modern, young multidisciplinary and multi-paradigm scientific platform involving nuclear medicine, neuroscience, neurophysiology, neuroendocrinology, neuroimmunology, etc., through the prism of fundamentally applied algorithms/tools/technologies for pathogenesis, diagnosis, treatment and prevention of neurodegenerative diseases. Cognitive brain science and longevity Homo sapiens: energy, quantum, biophysical and biochemical loss of cognitive brain controllability of aging processes. Circadian, electromagnetic, and nutriciological aging is the energy, quantum, biophysical, and biochemical loss of cognitive brain controllability of chronobiological processes associated with age-associated diseases (syndromes, symptoms). A new author’s multidisciplinary and multi-paradigm platform has been formed, through the prism of fundamental applied algorithms/tools/technologies for the pathogenesis, diagnosis, treatment and prevention of this neurodegeneration (Alzheimer’s disease, vascular dementia), which allows you to strategically simulate and predict the time (age) of onset of cognitive decline in Alzheimer’s disease. Homo sapiens: cognitive brains are biological, biophysical, neurophysiological, and medico-social information exchange paradigms. The achievement of research Romanchuk N. P. is the establishment of many genetic and epigenetic factors of cognitive decline and neurodegenerative diseases. Modern technologies of nuclear medicine make it possible to restore the structural-functional cognitive brain.

Estimated glomerular filtration rate and serum neurofilament light chain: Insight from National Health and Nutrition Examination Survey

The neurofilament light chain is a protein biomarker associated with neurodegenerative diseases. Neurofilament light chain levels may increase as kidney function declines due to reduced clearance. However, the relationship between estimated glomerular filtration rate (eGFR) and serum neurofilament light chain (sNfL) has not been extensively studied. Therefore, the objective of this study was to examine the association between eGFR and sNfL levels. Health survey data from 2071 eligible participants in the National Health and Nutrition Examination Survey (NHANES) were used in three multivariate-adjusted weighted linear regression models to analyze the correlation between eGFR and sNfL. Subsequently, segmental linear regression analysis was employed to determine the inflection point of eGFR. Finally, through subgroup analysis, we aimed to assess the impact of all covariates on the association between eGFR and sNfL. According to our results, sNfL levels decreased as eGFR increased. The segmental linear regression model analysis identified an inflection point at 59.9. When eGFR reached 59.9 or exceeded it, each unit increase in eGFR was associated with a 1 pg/mL decrease in sNfL (&amp;beta; = &amp;minus;0.1, P = 0.01). Furthermore, subgroup analysis revealed that hypertension exhibited a significant interaction with the association between eGFR and sNfL (P = 0.01). These findings suggest that eGFR holds promise as a potential marker for neurodegenerative disorders, and hypertension could affect this association to some extent. Moreover, these results could have significant implications for the early detection and prevention of neurodegenerative diseases in patients with kidney disease. However, further research is needed to corroborate these results and elucidate the underlying mechanisms.