Bacterial resistance is a naturally occurring process. However, bacterial antibiotic resistance has emerged as a major public health problem in recent years. The accumulation of antibiotics in the environment, including in wastewaters and drinking water, has contributed to the development of antibiotic resistant bacteria and the dissemination of antibiotic resistance genes (ARGs). Such can be justified by the growing consumption of antibiotics and their inadequate elimination. The conventional water treatments are ineffective in promoting the complete elimination of antibiotics and bacteria, mainly in removing ARGs. Therefore, ARGs can be horizontally transferred to other microorganisms within the aquatic environment, thus promoting the dissemination of antibiotic resistance. In this review, we discuss the efficiency of conventional water treatment processes in removing agents that can spread/stimulate the development of antibiotic resistance and the promising strategies for water remediation, mainly those based on nanotechnology and microalgae. Despite the potential of some of these approaches, the elimination of ARGs remains a challenge that requires further research. Moreover, the development of new processes must avoid the release of new contaminants for the environment, such as the chemicals resulting from nanomaterials synthesis, and consider the utilization of green and eco-friendly alternatives such as biogenic nanomaterials and microalgae-based technologies.

Accumulation of amyloid-beta (Aβ) in the brain is thought to derive from the impairment of Aβ clearance mechanisms rather than from its overproduction, which consequently contributes to the development of Alzheimer’s disease. The choroid plexus epithelial cells constitute an important clearance route for Aβ, either by facilitating its transport from the cerebrospinal fluid to the blood, or by synthesizing and secreting various proteins involved in Aβ degradation. Impaired choroid plexus synthesis, secretion, and transport of these Aβ-metabolizing enzymes have been therefore associated with the disruption of Aβ homeostasis and amyloid load. Factors such as aging, female gender, and circadian rhythm disturbances are related to the decline of choroid plexus functions that may be involved in the modulation of Aβ-clearance mechanisms. In this study, we investigated the impact of age, sex hormones, and circadian rhythm on the expression of Aβ scavengers such as apolipoprotein J, gelsolin, and transthyretin at the rat choroid plexus. Our results demonstrated that mRNA expression and both intracellular and secreted protein levels of the studied Aβ scavengers are age-, sex-, and circadian-dependent. These data suggest that the Aβ-degradation and clearance pathways at the choroid plexus, mediated by the presence of Aβ scavengers, might be compromised as a consequence of aging and circadian disturbances. These are important findings that enhance the understanding of Aβ-clearance-regulating mechanisms at the blood–cerebrospinal fluid barrier.