Cannabis sativa emerges as a noteworthy candidate for its medicinal potential, particularly in wound healing. This review article explores the efficacy of cannabis oil in reducing reactive oxygen species (ROS) during the healing of acute and chronic wounds, comparing it to the standard treatments. ROS, produced from various internal and external sources, play a crucial role in wound development by causing cell and tissue damage. Understanding the role of ROS on skin wounds is essential, as they act both as signaling molecules and contributors to oxidative damage. Cannabis oil, recognized for its antioxidant properties, may help mitigate oxidative damage by scavenging ROS and upregulating antioxidative mechanisms, potentially enhancing wound healing. This review emphasizes ongoing research and the future potential of cannabis oil in dermatological treatments, highlighted through clinical studies and patent updates. Despite its promising benefits, optimizing cannabis oil formulations for therapeutic applications remains a challenge, underscoring the need for further research to realize its medicinal capabilities in wounds.

The precise aetiology of Parkinson’s disease (PD) is still poorly understood, but it is thought to arise due to an intricate relationship between genes and the environment. Our study takes a unique approach to understanding the effect of environmental factors on the onset and progression of α-synuclein (aSyn) pathology, a key feature of PD, from the olfactory bulb (OB) to other brain regions. In the present study, we evaluated the time-dependent progression of PD-like pathology by administering rotenone intranasally for 5.5 months in C57BL/6 male mice. We performed olfactory and motor tests and examined the aSyn accumulation, glial cell activation and dopaminergic neurodegeneration after 3, 4 and 5.5 months of rotenone exposure by immunoblotting and immunofluorescence techniques. We observed a time-dependent progression of aSyn accumulation from the OB to other brain regions, including the mid-brain and cortex. Consistently, we observed a time-dependent behavioural impairment, OB atrophy, progression of aSyn pathology, neuroinflammation and neurodegeneration. Our findings also established a link between distinct astrocyte activation and dopaminergic (DAergic) activity. In conclusion, this chronic and progressive mouse model mimics the brain-first type of progression of PD-like pathology in some PD patients, opening the possibility for testing potential disease-modifying interventions. Graphical

The precise etiology of Parkinson’s disease (PD) is still poorly understood, but it is thought to arise due to an intricate relationship between genes and the environment. Our study takes a unique approach to understanding the effect of environmental factors on the onset and progression of α-synuclein (aSyn) pathology, a key feature of PD, from the olfactory bulb (OB) to other brain regions. In the present study, we evaluated the time-dependent progression of PD-like pathology by administering rotenone intranasally for 5.5 months in C57BL/6 male mice. We performed olfactory and motor tests and examined aSyn accumulation, glial cell activation, and dopaminergic (DAergic) neurodegeneration after 3, 4, and 5.5 months of rotenone exposure by immunoblotting and immunofluorescence techniques. We observed a time-dependent progression of aSyn accumulation from the OB to other brain regions, including the mid-brain and cortex. Consistently, we observed a time-dependent behavioral impairment, OB atrophy, progression of aSyn pathology, neuroinflammation, and neurodegeneration. Our findings also established a link between distinct astrocyte activation and DAergic activity. In conclusion, this chronic and progressive mouse model mimics the brain-first type of progression of PD-like pathology in some PD patients, opening the possibility for testing potential disease-modifying interventions.

Background: Alzheimer’s disease (AD) shows distinct differences between women and men in prevalence, disease progression, and therapeutic response. Women express a greater risk of AD onset, influenced by increased longevity and hormonal factors, and typically experience faster cognitive decline along with heightened susceptibility to AD-associated depression and anxiety. Current therapies—primarily cholinesterase inhibitors and memantine—offer only symptomatic relief without modifying disease progression. Objective: To review sex-specific differences in Alzheimer’s disease and evaluate the current understanding of therapeutic response variations between men and women, with an emphasis on identifying opportunities for sex-tailored interventions. Methods: A narrative review of the literature on AD prevalence, progression, and treatment outcomes across sexes was conducted. Particular attention was given to pharmacological therapies (cholinesterase inhibitors, memantine), lifestyle factors, and sex-specific risk determinants such as cardiovascular health and hormonal fluctuations. Results: Evidence suggests that women are more vulnerable to AD onset and progression compared to men. Limited studies indicate potential therapeutic advantages of specific medications for women, though robust, sex-stratified clinical trials remain lacking. Non-pharmacological strategies, including lifestyle adjustments in diet, exercise, and cognitive engagement, show promise in alleviating symptoms for both sexes. Conclusions: Sex differences significantly influence AD onset, clinical course, and therapeutic response. While current treatment remains largely non-disease-modifying, emerging sex-specific findings underscore the need for personalised medicine approaches. Further research is required to clarify sex specific mechanisms, optimise therapeutic strategies, and address disparities in care access, ultimately improving management of AD in both women and men.