Neurodegenerative diseases affect millions of people worldwide. Neurodegenerative diseases result from progressive damage to nerve cells in the brain or peripheral nervous system connections that are essential for cognition, coordination, strength, sensation, and mobility. Dysfunction of these brain and nerve functions is associated with Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Amyotrophic lateral sclerosis, and motor neuron disease. In addition to these, 50% of people living with HIV develop a spectrum of cognitive, motor, and/or mood problems collectively referred to as HIV-Associated Neurocognitive Disorders (HAND) despite the widespread use of a combination of antiretroviral therapies. Neuroinflammation and neurotransmitter systems have a pathological correlation and play a critical role in developing neurodegenerative diseases. Each of these diseases has a unique pattern of dysregulation of the neurotransmitter system, which has been attributed to different forms of cell-specific neuronal loss. In this review, we will focus on a discussion of the regulation of dopaminergic and cholinergic systems, which are more commonly disturbed in neurodegenerative disorders. Additionally, we will provide evidence for the hypothesis that disturbances in neurotransmission contribute to the neuronal loss observed in neurodegenerative disorders. Further, we will highlight the critical role of dopamine as a mediator of neuronal injury and loss in the context of NeuroHIV. This review will highlight the need to further investigate neurotransmission systems for their role in the etiology of neurodegenerative disorders.

The objective of this study was to evaluate the capacity of two bacterial strains isolated, cultivated, and purified from agricultural soils of Veracruz, Mexico, for biodegradation and mineralisation of malathion (diethyl 2-(dimethoxyphosphorothioyl) succinate) and α- and β-endosulfan (6,7,8,9,10,10-hexachloro-1,5,5a,6,9,9a-hexahydro-6-9-methano-2,4,3-benzodioxathiepine-3-oxide). The isolated bacterial strains were identified using biochemical and morphological characterization and the analysis of their 16S rDNA gene, as Enterobacter cloacae strain PMM16 (E1) and E. amnigenus strain XGL214 (M1). The E1 strain was able to degrade endosulfan, whereas the M1 strain was capable of degrading both pesticides. The E1 strain degraded 71.32% of α-endosulfan and 100% of β-endosulfan within 24 days. The absence of metabolites, such as endosulfan sulfate, endosulfan lactone, or endosulfan diol, would suggest degradation of endosulfan isomers through non-oxidative pathways. Malathion was completely eliminated by the M1 strain. The major metabolite was butanedioic acid. There was a time-dependent increase in bacterial biomass, typical of bacterial growth, correlated with the decrease in pesticide concentration. The CO₂ production also increased significantly with the addition of pesticides to the bacterial growth media, demonstrating that, under aerobic conditions, the bacteria utilized endosulfan and malathion as a carbon source. Here, two bacterial strains are shown to metabolize two toxic pesticides into non-toxic intermediates.

Prolonged exposure to HIV-1 transactivator of transcription (Tat) protein dysregulates monoamine transmission, a physiological change implicated as a key factor in promoting neurocognitive disorders among people living with HIV. We have demonstrated that in vivo expression of Tat in Tat transgenic mice decreases dopamine uptake through both dopamine transporter (DAT) and norepinephrine transporter (NET) in the prefrontal cortex. Further, our novel allosteric inhibitor of monoamine transporters, SRI-32743, has been shown to attenuate Tat-inhibited dopamine transport through DAT and alleviates Tat-potentiated cognitive impairments. The current study reports the pharmacological profiles of SRI-32743 in basal and Tat-induced inhibition of human NET (hNET) function. SRI-32743 exhibited less affinity for hNET binding than desipramine, a classical NET inhibitor, but displayed similar potency for inhibiting hDAT and hNET activity. SRI-32743 concentration-dependently increased hNET affinity for [³H]DA uptake but preserved the V_max of dopamine transport. SRI-32743 slowed the cocaine-mediated dissociation of [³H]Nisoxetine binding and reduced both [³H]DA and [³H]MPP+ efflux but did not affect d-amphetamine-mediated [³H]DA release through hNET. Finally, we determined that SRI-32743 attenuated a recombinant Tat_1–86-induced decrease in [³H]DA uptake via hNET. Our findings demonstrated that SRI-32743 allosterically disrupts the recombinant Tat_1–86–hNET interaction, suggesting a potential treatment for HIV-infected individuals with concurrent cocaine abuse.

Diversos estudios muestran el efecto de la temperatura en la bioacumulación de contaminantes en molus- cos bivalvos, pero la in uencia de esté factor en la bioacumulación de hidrocarburos (HC) en Crassostrea virginica no se ha reportado. En este trabajo se estudió el efecto de la temperatura sobre la acumulación de HC en C. virginica en condiciones controladas, la tasa de sobrevivencia (TS) y el desarrollo gametogénico. Se aplicaron cuatro tratamientos con diferentes temperaturas y concentración de HC: A (sin HC a 26 ◦C), B (sin HC a 30 ◦C), C (con HC a 26 ◦C) y D (con HC a 30 ◦C) y el control (sin HC a temperatura ambiente). Los resultados mostraron que el control y los tratamientos A y B tuvieron los valores más bajos de bioacumulación de HC con cantidades menores de 30 mg kg−1. En el tratamiento C se estimaron valores de acumulación de 83 mg kg−1. Mientras que en el tratamiento D se registraron los niveles más altos de HC con 118 mg kg−1 y la TS más baja (53 %). La TS mayor (93 %) se registró en el control y los tratamientos A y C. A nivel celular no se identi có ninguna patología, pero el desarrollo gonádico fue afectado por la presencia de HC y la temperatura de 30◦C, con escaso crecimiento gonadal, predominando organismos inde nidos. Las diferentes temperaturas no in uyeron en la bioacumulación de HC en los organismos, pero se observa efecto negativo en el desarrollo gametogénico y la TS.

One month of EcoHIV infection serves as a model of chronic HIV infection. Chronic exposure to EcoHIV viral proteins via direct interactions with dopamine and serotonin transporters (DAT and SERT) induces neuroadaptations, including neurotransmitter (NT, DA or serotonin) dysregulation and up- or downregulation of DAT and SERT function at synaptic terminals.