Dengue fever is the most important mosquito-borne viral disease in Southeast Asia. Insecticides remain the most effective vector control approach for Aedes mosquitoes. Four main classes of insecticides are widely used for mosquito control: organochlorines, organophosphates, pyrethroids and carbamates. Here, we review the distribution of dengue fever from 2000 to 2020 and its associated mortality in Southeast Asian countries, and we gather evidence on the trend of insecticide resistance and its distribution in these countries since 2000, summarising the mechanisms involved. The prevalence of resistance to these insecticides is increasing in Southeast Asia, and the mechanisms of resistance are reported to be associated with target site mutations, metabolic detoxification, reduced penetration of insecticides via the mosquito cuticle and behavioural changes of mosquitoes. Continuous monitoring of the status of resistance and searching for alternative control measures will be critical for minimising any unpredicted outbreaks and improving public health. This review also provides improved insights into the specific use of insecticides for effective control of mosquitoes in these dengue endemic countries.

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Parkinson's disease (PD) is the second most common neurodegenerative disorder that is known to cause progressive impairment of voluntary motor control [1]. The prevalence of PD has doubled over the past 3 decades, with an estimated 6.1 million individuals living with PD in 2016 [2]. The risk of developing PD increases with age, from 1% of the population older than 60 years to 5% of the population older than 85 years [3,4]. In PD patients, there is loss of dopaminergic neurons in substantia nigra pars compacta, which is crucial for normal movement coordination [5]. As such, PD patients suffer from motor symptoms including resting tremor, bradykinesia, postural instability, and rigidity. Additionally, nonmotor symptoms such as neurobehavioral complications, autonomic dysfunction, and sensory problems are commonly reported among PD patients [1]. Various cellular mechanisms including mitochondrial dysfunction, excitotoxicity, impaired autophagy, oxidative stress, accumulation of misfolded protein, and genetic mutations have been suggested to contribute to the neurodegeneration in PD [6,7].

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