Appearance Of Neurodegenerative Diseases Research Articles

Environmental pesticide exposure and Alzheimer's disease in southern Spain: A cross-sectional study

The intensive cultivation under plastic in southern Spain has made the agricultural model highly productive. Although strict regulations on pesticide usage exist, exposure to pesticides in the environment has been associated with an increased appearance of neurodegenerative diseases including Alzheimer's disease (AD). A cross-sectional study was performed to examine the prevalence and risk of AD related to pesticide exposure in Andalusia (Spain). We utilized the Odds Ratio statistical test to compare the prevalence rate of AD in the exposed and unexposed areas. 40,044 cases were collected from computerized hospital records between 2000 and 2021. Districts with higher pesticide use showed significantly higher prevalence rates and increased risk of developing AD, compared to those with lower pesticide use. These findings provide further evidence supporting an increased risk of AD following environmental exposure to pesticides at the level of the general population.

Mathematical and computational modeling of the role of homocysteine in the oxidative process and its influence in neuronal degenerative diseases

Degenerative neurological diseases, although common in the population, are difficult to diagnose. However, it is known that most of them are directly related to the so-called oxidative stress. Understanding and evaluating how this process takes place is of great interest and, in this sense, this work extends the existing mathematical and computational models for the oxidative stress process (REIS, 2005; REIS et al., 2006; VIANNA, 2005; VIANNA; REIS; CARVALHO, 2012), incorporating an aspect not previously evaluated, the influence of homocysteine indices on the oxidants present in this process. The results indicate that hyperhomocysteinemia can in fact cause oxidative stress and consequent neuronal death, leading to the appearance of neurodegenerative diseases.

Genetic Aspects of Glial Cells Regarding Neurodegenerative Diseases.

Glial cells (also known as glia or neuroglia) are structures which are found in large numbers throughout the nervous system, fulfilling multiple functions, such as regulating the synapses, providing structure, support and nutrition, contributing towards the immune response and tissue oxygenation. Knowledge regarding glial cells has increased during the last few years, since Virchow defined them as supporting connective tissue, followed by Ramón y Cajal who described them as tissue in themselves, until today when a first order physiological role has been recognised for them and a leading role in the appearance and progression of various pathological processes, primarily in the group of Neurodegenerative Diseases (ND). The ND represents a group of pathologies which gradually cause the degeneration of nervous tissue, have a broad spectrum regarding their appearance and, in some cases, are the direct consequence of genetic alterations leading to physiological changes in the nervous system. The present article has thus been aimed at describing glial cells' genetic interaction with ND through a systemic review of the pertinent literature. The mechanisms through which the different classes of glial cells become involved in the appearance of ND are poorly understood; however, evidence indicates that their role could be a critical factor in these pathologies' appearance, regulation and chronicity, these being largely determined by different types of cellular interactions and interaction with the microenvironment. This review shows that ND genetics regarding glial cells' cellular, molecular and genetic functioning represents a complex and understudied process; studying these factors could be a key step for ascertaining the origin of these pathologies, thereby leading to more effective therapies being developed.

Brain aging and neurodegeneration: from a mitochondrial point of view.

Aging is defined as a progressive time‐related accumulation of changes responsible for or at least involved in the increased susceptibility to disease and death. The brain seems to be particularly sensitive to the aging process since the appearance of neurodegenerative diseases, including Alzheimer's disease, is exponential with the increasing age. Mitochondria were placed at the center of the ‘free‐radical theory of aging’, because these paramount organelles are not only the main producers of energy in the cells, but also to main source of reactive oxygen species. Thus, in this review, we aim to look at brain aging processes from a mitochondrial point of view by asking: (i) What happens to brain mitochondrial bioenergetics and dynamics during aging? (ii) Why is the brain so sensitive to the age‐related mitochondrial impairments? (iii) Is there a sex difference in the age‐induced mitochondrial dysfunction? Understanding mitochondrial physiology in the context of brain aging may help identify therapeutic targets against neurodegeneration. This article is part of a series “Beyond Amyloid”.

Structural and Functional Characteristics of Oxysterol 7α-Hydroxylase with Amino-Acid Substitution R486C and Their Relation to the Appearance of Neurodegenerative Diseases

The influence of the amino-acid substitution Arg486Cys on the conformational stability of recombinant cytochrome P450 7B1 (CYP7B1, oxysterol 7α-hydroxylase) was studied. The single base change was shown to decrease the free energy of the transition of the heme-protein from its native state to a denatured one, which pointed to a lower thermodynamic stability for the mutant form of the enzyme. This could be the cause of the metabolic disruption of neurosteroids and, as a consequence, the appearance of neurodegenerative diseases.

Is electron-transfer from glutamate receptors or other plasma membrane ionic channels involved in oxidative stress and neurodegenerative diseases?

There is theoretical evidence that biopolymers such as proteins can have semiconductor properties, with electrons (and holes) that can move inside the macromolecule. Double layers of charge can thus be formed at the plasma membrane protein interface with the electrolytes. Electron-transfer can occur at such interfaces too, and electrons can participate in charge transport processes across the biopolymer from one side of the plasma membrane to the other. These phenomena are studied here in the pathological case when the average equilibrium in the electron-transfer process at the cytoplasmic interface suffers a continued offset that leads to free-radical formation inside the cell. This would help in the long term to increase oxidative stress inside the cell, and would thus contribute to the appearance of neurodegenerative diseases.