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.

Mozambique possesses great biological diversity, with approximately 5500 plant species. Around 90% of its population uses natural resources for food and traditional medicine, being miombo forests serving as key providers for rural communities. The trade of medicinal plants also constitutes a significant economic activity for both rural and urban households. This study aims to review ethnobotanical and ethnopharmacological studies on medicinal plants in Mozambique and explore their agricultural and conservation potential. Articles published between 2010 and 2024 were included and identified 472 medicinal plant species, 400 of which were classified to species or genus level, spanning 277 genera and 93 botanical families. The most cited families include Leguminosae (61 species), Euphorbiaceae (20), and Combretaceae (17). Notable species are Momordica balsamina, Sclerocarya birrea, Annona senegalensis, and Cassia abbreviata. Sixteen in vitro studies explored medicinal plants’ antibacterial, antimycobacterial, antimicrobial, anticancer, and antimalarial properties. Prominent results were shown by Maerua edulis (tuberculosis), Tabernaemontana elegans (malaria), and Momordica balsamina (cancer). This work underscores the critical role of natural resources in Mozambique’s primary healthcare system and highlights their agricultural and economic potential. As the first comprehensive compilation of commonly used medicinal plants in the country, it calls for sustainable cultivation practices and further research to enhance their use and benefits.

Imidacloprid (IMI), the most widely used worldwide neonicotinoid biocide, produces cognitive disorders after repeated and single treatment. However, little was studied about the possible mechanisms that produce this effect. Cholinergic neurotransmission regulates cognitive function. Most cholinergic neuronal bodies are present in the basal forebrain (BF), regulating memory and learning process, and their dysfunction or loss produces cognition decline. BF SN56 cholinergic wild-type or acetylcholinesterase (AChE), β-amyloid-precursor-protein (βAPP), Tau, glycogen-synthase-kinase-3-beta (GSK3β), beta-site-amyloid-precursor-protein-cleaving enzyme 1 (BACE1), and/or nuclear-factor-erythroid-2-related-factor-2 (NRF2) silenced cells were treated for 1 and 14 days with IMI (1 μM-800 μM) with or without recombinant heat-shock-protein-70 (rHSP70), recombinant proteasome 20S (rP20S) and with or without N-acetyl-cysteine (NAC) to determine the possible mechanisms that mediate this effect. IMI treatment for 1 and 14 days altered cholinergic transmission through AChE inhibition, and triggered cell death partially through oxidative stress generation, AChE-S overexpression, HSP70 downregulation, P20S inhibition, and Aβ and Tau peptides accumulation. IMI produced oxidative stress through reactive oxygen species production and antioxidant NRF2 pathway downregulation, and induced Aβ and Tau accumulation through BACE1, GSK3β, HSP70, and P20S dysfunction. These results may assist in determining the mechanisms that produce cognitive dysfunction observed following IMI exposure and provide new therapeutic tools.