Pubmed (TSA) du 08/02/26
1. Almughyiri S. Understanding pain experiences in individuals with developmental disabilities in Saudi Arabia: A qualitative interview study. Res Dev Disabil;2026 (Feb 6);170:105242.
Research is limited on presenting optimal insights into the pain experiences of individuals with development disabilities (DD). Due to the group’s insufficient communication skills, experts find it challenging to accurately assess pain. As a result, individuals with DDs often encounter the consequences of undiagnosed pain. A similar risk tends to increase in certain countries, particularly the Kingdom of Saudi Arabia (KSA), considering the impact of distinct cultural and social characteristics that define pain experiences. This qualitative research, utilizing an exploratory research design and an interpretivist research philosophy, aims to critically examine pain experiences in individuals with DDs in Saudi Arabia. Semi-structured interviews were conducted with 25 healthcare professionals, family caregivers, physiotherapists, and special education teachers. Important themes identified in the current research include diverse pain interpretations, the implications of persistent behavioral changes, challenges in identifying different types of pain, pain management as an ongoing, context-specific process, and systemic and cultural factors that determine pain management in individuals with DDs in KSA. A relevant aspect emerging in the study is associated with comprehending the varied nuances of pain experiences of individuals with DDs.
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2. Lu Q, Tian C, Li L, Liu X, Liu J, He Y, Zhang A, Wang W. Nicotinamide mononucleotide rescues perinatal arsenic-induced autism-like behaviours via modulation of NAD+ metabolism in mice. Ecotoxicol Environ Saf;2026 (Feb 6);311:119840.
Recent epidemiological studies have indicated that exposure to arsenic (As), particularly during key phases of central nervous system development, may be an environmental risk factor for autism spectrum disorder (ASD). While nicotinamide mononucleotide (NMN) confers neuroprotection by elevating tissue nicotinamide adenine dinucleotide (NAD+), its efficacy against ASD pathophysiology remains unexplored. Here, a mouse model of perinatal As exposure (1.2 mg/kg/d) and NMN intervention (500 mg/L) was employed, and NMN was found to rescue As-induced NAD+ depletion in offspring brain tissues. This restoration coincided with increased synaptic density in the cortex and significant attenuation of autism-like behavioural phenotypes. Additionally, NMN restored As-induced intestinal dysbiosis and enriched beneficial genera including Lactobacillus and Akkermansia, restoring the Firmicutes/Bacteroidetes ratio. Consistently, As exposure exacerbated inflammatory damage in colonic tissues, elevated pro-inflammatory cytokine levels in serum, and activated cortical microglia and astrocytes. In contrast, NMN supplementation markedly alleviated these inflammatory and neuroimmune disturbances. Notably, NMN also increased Clostridium species, which synthesise vitamin B3 (VB3), a precursor of NAD+ . Moreover, the intervention alleviated the As-induced disruption of colonic epithelial tight junctions and polarity, while concomitantly upregulating NAD+ synthase and NAD+ precursor transporter proteins that were inhibited by As. Collectively, these actions restored perinatal As-induced NAD+ deficits in offspring, providing novel mechanistic insights into the therapeutic potential of NMN against As-driven autism-like phenotypes. These findings offer a foundation for dietary supplementation with NMN as a strategy for clinical translation.
