Environmental pollutants’ (EPs) amount and diversity have increased in recent years due to anthropogenic activity. Several neurodegenerative diseases (NDs) are theorized to be related to EPs, as their incidence has increased in a similar way to human EPs exposure and they reproduce the main ND hallmarks. EPs induce several neurotoxic effects, including accumulation and gradual deposition of misfolded toxic proteins, producing neuronal malfunction and cell death. Cells possess different mechanisms to eliminate these toxic proteins, including heat shock proteins (HSPs) and the proteasome system. The accumulation and deleterious effects of toxic proteins are induced through HSPs and disruption of proteasome proteins’ homeostatic function by exposure to EPs. A therapeutic approach has been proposed to reduce accumulation of toxic proteins through treatment with recombinant HSPs/proteasome or the use of compounds that increase their expression or activity. Our aim is to review the current literature on NDs related to EP exposure and their relationship with the disruption of the proteasome system and HSPs, as well as to discuss the toxic effects of dysfunction of HSPs and proteasome and the contradictory effects described in the literature. Lastly, we cover the therapeutic use of developed drugs and recombinant proteasome/HSPs to eliminate toxic proteins and prevent/treat EP-induced neurodegeneration.

B. crassifolia is a species that grows in various areas of Latin America. It was known to be useful for the treatment of different human ailments. The present work evaluated the neuropharmacological and analgesic effects of hydroalcoholic and dichloromethane extracts of B. crassifolia. The effect on the central nervous system (CNS) of both extracts obtained from bark, administered by the intraperitoneal route in mice, was evaluated by different tests: spontaneous motor activity, hole-board, motor coordination, pentobarbital induced hypnosis, and rectal temperature. Analgesic activity was evaluated using a hot plate test. Phytochemical analysis was performed by high-performance liquid chromatography (HPLC) using reversed-phase and gradient of elution. The hydroalcoholic extract (dose 0.5 g dry plant/kg weigh) administration caused an important reduction of the head-dipping response in the hole board test. A decrease in spontaneous motor activity test and a disturbance of motor coordination in the rotarod test was observed. The hydroalcoholic extract produced a significant prolongation of pentobarbital induced sleeping time. This extract prevented hot plate test induced nociception. The phytochemical analysis revealed the presence of catechin, epicatechin, and procyanidin B12. Therefore, this study revealed that the hydroalcoholic extract of B. crassifolia possesses analgesic and sedative CNS activity.

Chlorpyrifos (CPF) biocide, exposure to which is mainly produced in the human population through diet, induces several neurotoxic effects. CPF single and repeated exposure induces memory and learning disorders, although the mechanisms that produce these outcomes are complex and not well understood. CPF treatment (single and repeated) of cholinergic septal SN56 cells induced an increase in phosphorylated-P38α levels that led to WNT/β-Catenin and NGF/P75^NTR/TrkA pathways disruption and cell death. These results provide new knowledge on the mechanisms that mediate CPF basal forebrain cholinergic neuronal loss induced by CPF single and repeated exposure and can help unravel the way through which this compound produces cognitive decline and develop efficient treatments against these effects.

Chlorpyrifos, a broad-spectrum insecticide categorized within the organophosphate family, is recognized for its potent inhibition of the enzyme Acetylcholinesterase (AChE), resulting in the manifestation of cholinergic syndrome in humans. Beyond its well-established toxicity in the central nervous system, recent studies have explored additional pathways through which this pesticide may adversely impact human health. Breast cancer, characterized by the uncontrolled proliferation of epithelial cells in the mammary gland, stands as the most diagnosed cancer in women and is a leading global cause of female cancer-related deaths. Chlorpyrifos, extensively employed worldwide for pest control in agriculture, domestic settings, and industries, has notably faced recent bans in the European Union, marking a significant regulatory shift. This bibliographical review aims to unravel the intricate mechanisms by which chlorpyrifos may contribute to the development of breast cancer. Collating findings from human studies, as well as in vitro and in vivo research spanning the past decade, the review sheds light on chlorpyrifos as a potent endocrine disruptor. It influences female sex hormones, exhibits estrogenic effects on breast cancer cells, and induces alterations in breast tissue. Additionally, chlorpyrifos acts as an agonist of Estrogen Receptor α(ERα) and Aryl hydrocarbon Receptor (AhR), contributing to cell proliferation, oxidative stress, and engaging epigenetic and angiogenic mechanisms. This comprehensive review underscores the compelling association between chlorpyrifos exposure and mammary cancer. It emphasizes the urgent need for further research on pesticide usage to mitigate potential adverse health consequences.