Prevalence Of Neurodegenerative Disorders Research Articles

Neuron Foundry Mach 8: A Concept of Multi-modal Neuro-supportive Energy Therapy Device for Treating Neurodegenerative Disorders

The prevalence of neurodegenerative disorders is rising as the population ages, and many ailments, such as depression, Parkinson’s disease, Alzheimer’s disease, autism spectrum disorder, and multiple sclerosis, have intricate underlying mechanisms that are still poorly understood. The Neuron Foundry Mach 8 is a multi-modal neuro-supportive energy therapy device designed to treat neurodegenerative disorders through daily sessions. This device proposes to deliver safe and controlled energy therapy through multiple therapeutic pathways, including stimulating brain mitochondrial energy, supporting homeostasis within the brain’s immune system, increasing melatonin production within neuronal mitochondria, and triggering cellular communication through the brain’s white matter. By combining these unique energy-based treatments, this device holds promising potential for slowing, stopping, reversing, or at least reducing the effects of neurodegenerative diseases.

Metformin, Cognitive Function, and Changes in the Gut Microbiome.

The decline in cognitive function and the prevalence of neurodegenerative disorders are among the most serious threats to health in old age. The prevalence of dementia has reached 50 million people worldwide and has become a major public health problem. The causes of age-related cognitive impairment are multiple, complex, and difficult to determine. However, type 2 diabetes (T2D) is linked to an enhanced risk of cognitive impairment and dementia. Human studies have shown that patients with T2D exhibit dysbiosis of the gut microbiota. This dysbiosis may contribute to the development of insulin resistance and increased plasma lipopolysaccharide concentrations. Metformin medication mimics some of the benefits of calorie restriction and physical activity, such as greater insulin sensitivity and decreased cholesterol levels, and hence may also have a positive impact on aging in humans. According to recent human investigations, metformin might partially restore gut dysbiosis related to T2D. Likewise, some studies showed that metformin reduced the risk of dementia and improved cognition, although not all studies are concordant. Therefore, this review focused on those human studies describing the effects of metformin on the gut microbiome (specifically the changes in taxonomy, function, and circulating metabolomics), the changes in cognitive function, and their possible bidirectional implications.

Risk of neurodegenerative disease due to tau phosphorylation changes and arsenic exposure via drinking water.

It is estimated that around 140 million people are drinking highly contaminated water with arsenic (As) as a natural earth's crust component. On the other hand, the prevalence of neurodegenerative disorders, especially Alzheimer's disease, is constantly increasing. The aim of the present study was to investigate the correlation between oral arsenic trioxide exposure and its impact on tau protein phosphorylation at Ser262. Fifty-four male mice were randomly divided into three groups and were freely accessed to food and contaminated water of 1 and 10ppm arsenic trioxide for 3months, except for control subjects. At the end of each month, As concentration and tau phosphorylation were checked with graphite furnace atomic absorption spectrometer and western blot analysis, respectively. Surprisingly, it was observed that the amount of measured brain arsenic in 10ppm-exposed subjects was significantly increased after 3months (P-value ˂ 0.0001). The significant changes in tau phosphorylation were not seen in the 1ppm-exposed subjects, and it was observed that Ser262 phosphorylation significantly increased after 2 and 3months in the 10ppm group (P-value < 0.05). Our results demonstrated that arsenic accumulated in the brain time-dependently and increased Ser262 tau phosphorylation, which is very important in several tauopathies. In conclusion, it could be inferred that environmental arsenic exposure even at very low concentrations could be considered as a reason for increasing the risk of developing neurodegenerative disease.

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

In a constantly aging population, the prevalence of neurodegenerative disorders is expected to rise. Understanding disease mechanisms is the key to find preventive and curative measures. The most effective way to achieve this is through direct examination of diseased and healthy brain tissue. The authors present a protocol to obtain, process, characterize and store good quality brain tissue donated by individuals registered in an antemortem brain donation program. The donation program includes a face-to-face empathic approach to people, a collection of complementary clinical, biological, social and lifestyle information and serial multi-dimensional assessments over time to track individual trajectories of normal aging and cognitive decline. Since many neurological diseases are asymmetrical, our brain bank offers a unique protocol for slicing fresh specimens. Brain sections of both hemispheres are alternately frozen (at -80 °C) or fixed in formalin; a fixed slice on one hemisphere corresponds to a frozen one on the other hemisphere. With this approach, a complete histological characterization of all frozen material can be obtained, and omics studies can be performed on histologically well-defined tissues from both hemispheres thus offering a more complete assessment of neurodegenerative disease mechanisms. Correct and definite diagnosis of these diseases can only be achieved by combining the clinical syndrome with the neuropathological evaluation, which often adds important etiological clues necessary to interpret the pathogenesis. This method can be time consuming, expensive and limited as it only covers a limited geographical area. Regardless of its limitations, the high degree of characterization it provides can be rewarding. Our ultimate goal is to establish the first Italian Brain Bank, all the while emphasizing the importance of neuropathologically verified epidemiological studies.

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains.

In a constantly aging population, the prevalence of neurodegenerative disorders is expected to rise. Understanding disease mechanisms is the key to find preventive and curative measures. The most effective way to achieve this is through direct examination of diseased and healthy brain tissue. The authors present a protocol to obtain, process, characterize and store good quality brain tissue donated by individuals registered in an antemortem brain donation program. The donation program includes a face-to-face empathic approach to people, a collection of complementary clinical, biological, social and lifestyle information and serial multi-dimensional assessments over time to track individual trajectories of normal aging and cognitive decline. Since many neurological diseases are asymmetrical, our brain bank offers a unique protocol for slicing fresh specimens. Brain sections of both hemispheres are alternately frozen (at -80 °C) or fixed in formalin; a fixed slice on one hemisphere corresponds to a frozen one on the other hemisphere. With this approach, a complete histological characterization of all frozen material can be obtained, and omics studies can be performed on histologically well-defined tissues from both hemispheres thus offering a more complete assessment of neurodegenerative disease mechanisms. Correct and definite diagnosis of these diseases can only be achieved by combining the clinical syndrome with the neuropathological evaluation, which often adds important etiological clues necessary to interpret the pathogenesis. This method can be time consuming, expensive and limited as it only covers a limited geographical area. Regardless of its limitations, the high degree of characterization it provides can be rewarding. Our ultimate goal is to establish the first Italian Brain Bank, all the while emphasizing the importance of neuropathologically verified epidemiological studies.

Neuroprotective Natural Molecules, From Food to Brain.

The prevalence of neurodegenerative disorders is increasing; however, an effective neuroprotective treatment is still remaining. Nutrition plays an important role in neuroprotection as recently shown by epidemiological and biochemical studies which identified food components as promising therapeutic agents. Neuroprotection includes mechanisms such as activation of specific receptors, changes in enzymatic neuronal activity, and synthesis and secretion of different bioactive molecules. All these mechanisms are focused on preventing neuronal damage and alleviating the consequences of massive cell loss. Some neuropathological disorders selectively affect to particular neuronal populations, thus is important to know their neurochemical and anatomical properties in order to design effective therapies. Although the design of such treatments would be specific to neuronal groups sensible to damage, the effect would have an impact in the whole nervous system. The difficult overcoming of the blood brain barrier has hampered the development of efficient therapies for prevention or protection. This structure is a physical, enzymatic, and influx barrier that efficiently protects the brain from exogenous molecules. Therefore, the development of new strategies, like nanocarriers, that help to promote the access of neuroprotective molecules to the brain, is needed for providing more effective therapies for the disorders of the central nervous system (CNS). In order both to trace the success of these nanoplatforms on the release of the bioactive cargo in the CNS and determinate the concentration at trace levels of targets biomolecules by analytical chemistry and concretely separation instrumental techniques, constitute an essential tool. Currently, these techniques are used for the determination and identification of natural neuroprotective molecules in complex matrixes at different concentration levels. Separation techniques such as chromatography and capillary electrophoresis (CE), using optical and/or mass spectrometry (MS) detectors, provide multiples combinations for the quantitative and qualitative analysis at basal levels or higher concentrations of bioactive analytes in biological samples. Bearing this in mind, the development of food neuroprotective molecules as brain therapeutic agents is a complex task that requires the intimate collaboration and engagement of different disciplines for a successful outcome. In this sense, this work reviews the new advances achieved in the area toward a better understanding of the current state of the art and highlights promising approaches for brain neuroprotection.

Methods to Study Changes in Inherent Protein Aggregation with Age in &lt;em&gt;Caenorhabditis elegans&lt;/em&gt;

In the last decades, the prevalence of neurodegenerative disorders, such as Alzheimer's disease (AD) and Parkinson's disease (PD), has grown. These age-associated disorders are characterized by the appearance of protein aggregates with fibrillary structure in the brains of these patients. Exactly why normally soluble proteins undergo an aggregation process remains poorly understood. The discovery that protein aggregation is not limited to disease processes and instead part of the normal aging process enables the study of the molecular and cellular mechanisms that regulate protein aggregation, without using ectopically expressed human disease-associated proteins. Here we describe methodologies to examine inherent protein aggregation in Caenorhabditis elegans through complementary approaches. First, we examine how to grow large numbers of age-synchronized C. elegans to obtain aged animals and we present the biochemical procedures to isolate highly-insoluble-large aggregates. In combination with a targeted genetic knockdown, it is possible to dissect the role of a gene of interest in promoting or preventing age-dependent protein aggregation by using either a comprehensive analysis with quantitative mass spectrometry or a candidate-based analysis with antibodies. These findings are then confirmed by in vivo analysis with transgenic animals expressing fluorescent-tagged aggregation-prone proteins. These methods should help clarify why certain proteins are prone to aggregate with age and ultimately how to keep these proteins fully functional.

Translational Neurodegeneration, a platform to share knowledge and experience in translational study of neurodegenerative diseases

Translational Neurodegeneration, a platform to share knowledge and experience in translational study of neurodegenerative diseases

Multiprotein Deposits in Neurodegenerative Disorders: Our Experience in the Tissue Brain Bank of Navarra

The prevalence of neurodegenerative disorders increases dramatically with advancing age. Although in recent decades the study of many neurodegenerative disorders has evolved greatly, the concept of neurodegeneration still remains elusive. Although neurodegenerative disorders are classified according to the major components of protein deposits, coexpression of several abnormal proteins in the brain tissue is more common than that was previously thought. The aim of this report is to describe the type of protein deposits found in brains with neuropathological diagnosis of neurodegenerative disease. The report shows the experience obtained in the Brain Bank of Navarra (Spain). The target population for this retrospective descriptive study comprised 178 brains autopsied in the "Hospital of Navarra" in Pamplona between 1994 and 2004 and 201 brains donated to the Brain Bank of Pamplona between 2004 and 2009. The diagnosis of the 201 brains from the Brain Bank was 62 (30.8%) Alzheimer's disease (AD), 43 (21.3%) multiprotein deposit, 31 (15.4%) α-synucleinopathies, 31 (15.4%) frontotemporal lobar degeneration (FTLD), 17 (8.4%) tauopathies, 9 (4.4%) prion disease, 6 (2.9%) vascular dementia (VD), and 2 (0.9%) Huntington's disease. Among the 43 cases with multiprotein deposits, we found 35 brains with deposits of 3 proteins (tau, β-amyloid, and α-synuclein). In these two series of brains, the high incidence of deposition of multiple proteins in neurodegenerative disorders is shown. Our results are in agreement with previous findings showing that tau, β-amyloid, and α-synuclein are the proteins most frequently deposited together.

MicroRNAs: novel therapeutic targets in neurodegenerative diseases

The prevalence of neurodegenerative disorders is rising steadily as human life expectancy increases. However, limited knowledge of the molecular basis of disease pathogenesis is a major hurdle in the identification of drug targets and development of therapeutic strategies for these largely incurable disorders. Recently, differential expression of endogenous regulatory small RNAs, known as 'microRNAs' (miRNAs), in patients of Alzheimer's disease, Parkinson's disease and models of ataxia suggest that they might have key regulatory roles in neurodegeneration. miRNAs that can target known mediators of neurodegeneration offer potential therapeutic targets. Our bioinformatic analysis suggests novel miRNA-target interactions that could potentially influence neurodegeneration. The recent development of molecules that alter miRNA expression promises valuable tools that will enhance the therapeutic potential of miRNAs.

Prevalence of Parkinson’s disease in Korea

The prevalence of neurodegenerative disorders is not well documented in Korea. We assessed the prevalence of Parkinson’s disease in an elderly population in a newly industrialized city in a rural region. Subjects for this study were randomly selected from a community-based cohort study. The sample in the cohort represented approximately 1.3% (4700) of 362 625 adults (age > 18 years) listed in the city register in 1998. Among this group, 4218 subjects (1086 subjects aged > 60 years) agreed to be interviewed and underwent a physical examination and neuropsychological tests administered by a neurologist and neuropsychologist. All participants were examined. Participants who had bradykinesia and at least one other possible cardinal sign of parkinsonism at the neurologic screening, and those who reported that they had Parkinson’s disease, or were taking antiparkinsonian drugs were identified. In our study, 16 subjects showed evidence of Parkinson’s disease. The prevalence in this population was 0.37%. Prevalence increased with age, and prevalence was 1.47% for those aged older than 60 years. Postural instability and gait disturbance were more common in the older age group. The results of neuropsychological tests were as follows: (1) only two subjects had low scores (<20) in the Korea-version mini-mental status examination; (2) seven subjects scored 0.5, one subject scored 2 and the other eight subjects scored 0 in the clinical dementia rating. The results of our prevalence study are similar to those of studies carried out in Western countries. Age is a risk factor for Parkinson’s disease in Korea.

Neurodegenerative and other chronic disorders among people aged 75 years and over in the community.

To assess age-related disease patterns in the older population in the community, especially the prevalence of neurodegenerative disorders and their association with systemic and vascular diseases. Cross-sectional, community-based study. Area served by the Central Sydney Area Health Service, August 1991 to March 1994. 647 people aged 75 years or over, living in the community; 537 (83%) underwent medical assessment. Clinician diagnoses of chronic disease, including neurodegenerative disorders (cognitive and visual impairment, gait ataxia and slowing, dementia and Parkinson's disease); arteriopathy score; age-related trends; and correlations among diagnoses and arteriopathy score. Subjects had mean age of 81.0 years (range, 75-97). The most common diagnosis was arthritis (women, 73%; men, 68%), while the most common neurodegenerative diagnoses were gait ataxia (women, 57%; men, 42%), visual impairment (women, 40%; men, 45%) and cognitive impairment (women, 39%; men, 36%). Neurodegenerative diagnoses increased significantly in prevalence with increasing age, while most systemic diseases tended to decrease, although not significantly. Dementia was diagnosed in 92 subjects (17%), with Alzheimer's disease being the most common cause, but many having multiple causes. Significant correlations were found between neurodegenerative diagnoses and between the arteriopathy score and stroke, but not neurodegenerative diagnoses. The increase in comorbidities in the older population arises from an age-related increase in neurodegenerative disorders. These form a cluster suggesting a common aetiologic process which is not arteriopathic.