Epidemiology of dengue fever has substantially changed over the years with respect to prevalent strains, affected geographical locations and severity of disease. Mosquito vectors show variable response in terms of susceptibility to four different serotypes of dengue virus. Although studies have postulated that, the vectors Ae. aegypti and Ae. albopictus are crucial for transmission of dengue virus, comparative efficacy of these species for viral transmission and tolerance is still enigmatic. In this study, these two vectors were infected orally with four serotypes of the dengue virus viz. DENV-1 to DENV-4 and their co-infection. It was observed that Ae. aegypti harbors multiple serotype infections more efficiently than Ae. albopictus. We suggest that transovarial transmission is of low importance in the epidemiology of the virus due to low infection rates in the filial generation, and also that reduced fecundity and fertility in both vectors after dengue virus infection affect the ecology of the pathogen.Mosaicism, the presence of genomic differences between cells due to post-zygotic somatic mutations, is widespread in the human body, including within the brain. A role for this in neurodegenerative diseases has long been hypothesised, and technical developments are now allowing the question to be addressed in detail. The rapidly accumulating evidence is discussed in this review, with a focus on recent developments. Somatic mutations of numerous types may occur, including single nucleotide variants (SNVs), copy number variants (CNVs), and retrotransposon insertions. They could act as initiators or risk factors, especially if they arise in development, although they could also result from the disease process, potentially contributing to progression. In common sporadic neurodegenerative disorders, relevant mutations have been reported in synucleinopathies, comprising somatic gains of SNCA in Parkinson's disease and multiple system atrophy, and in Alzheimer's disease, where a novel recombination mechanism leading to somatic variants of APP, as well as an excess of somatic SNVs affecting tau phosphorylation, have been reported. In Mendelian repeat expansion disorders, mosaicism due to somatic instability, first detected 25 years ago, has come to the forefront. Brain somatic SNVs occur in DNA repair disorders, and there is evidence for a role of several ALS genes in DNA repair. While numerous challenges, and need for further validation, remain, this new, or perhaps rediscovered, area of research has the potential to transform our understanding of neurodegeneration.Inflammation has been linked to the development of nonmotor symptoms in Parkinson's disease (PD), which greatly impact patients' quality of life and can often precede motor symptoms. Suitable animal models are critical for our understanding of the mechanisms underlying disease and the associated prodromal disturbances. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkey model is commonly seen as a "gold standard" model that closely mimics the clinical motor symptoms and the nigrostriatal dopaminergic loss of PD, however MPTP toxicity extends to other nondopaminergic regions. Yet, there are limited reports monitoring the MPTP-induced progressive central and peripheral inflammation as well as other nonmotor symptoms such as gastrointestinal function and microbiota. We report 5 cases of progressive parkinsonism in non-human primates to gain a broader understanding of MPTP-induced central and peripheral inflammatory dysfunction to understand the potential role of inflammation in prodnfirmation and extension of these findings. Fluvastatin If these findings reflect potential differences in humans, these sex differences have significant implications for therapeutic development of inflammatory targets in the clinic.Epilepsy affects all ages, races, genders, and socioeconomic groups. In about one third of patients, epilepsy is uncontrolled with current medications, leaving a vast need for improved therapies. The causes of epilepsy are diverse and not always known but one gene mutated in a small subpopulation of patients is phosphatase and tensin homolog (PTEN). Moreover, focal cortical dysplasia, which constitutes a large fraction of refractory epilepsies, has been associated with signaling defects downstream of PTEN. So far, most preclinical attempts to reverse PTEN deficiency-associated neurological deficits have focused on mTOR, a signaling hub several steps downstream of PTEN. Phosphoinositide 3-kinases (PI3Ks), by contrast, are the direct enzymatic counteractors of PTEN, and thus may be alternative treatment targets. PI3K activity is mediated by four different PI3K catalytic isoforms. Studies in cancer, where PTEN is commonly mutated, have demonstrated that inhibition of only one isoform, p110β, reduces progression of PTEN-deficient tumors. Importantly, inhibition of a single PI3K isoform leaves critical functions of general PI3K signaling throughout the body intact. Here, we show that this disease mechanism-targeted strategy borrowed from cancer research rescues or ameliorates neuronal phenotypes in male and female mice with neuron-specific PTEN deficiency. These phenotypes include cell signaling defects, protein synthesis aberrations, seizures, and cortical dysplasia. Of note, p110β is also dysregulated and a promising treatment target in the intellectual disability Fragile X syndrome, pointing towards a shared biological mechanism that is therapeutically targetable in neurodevelopmental disorders of different etiologies. Overall, this work advocates for further assessment of p110β inhibition not only in PTEN deficiency-associated neurodevelopmental diseases but also other brain disorders characterized by defects in the PI3K/mTOR pathway. The Preparedness Plan for Surveillance and Interventions on Emerging Vector-Borne Diseases (VBDs) in Southern Switzerland outlines the strategy for preventing and managing potential outbreaks, as well as the surveillance and control activities with a specific focus on Aedes-borne diseases transmitted by Aedes albopictus mosquitoes. The objective of the plan is to provide Public Health Authorities with a framework of preventive and control measures according to the situation and level of epidemic risks. The plan is divided into various phases representing the different steps for all potential situations, ranging from no vectors and no transmission risk to epidemic levels with multiple autochthonous/local cases of hospitalization (and deaths) until the end of the epidemic. An algorithm presents how decisions are taken to move from one phase of the plan to another, with detailed activities for different partners and strategies for each specific phase. The different phases of the plan include activities on disease surveillance and clinical case management, on vector surveillance and control, communication and coordination of activities.