Migraine is the most common form of headache disorder globally. The etiology of migraine is multifactorial, with genetic components and environmental interactions considered to be the main causal factors. Some researchers postulate that deficits in mitochondrial energy reserves can cause migraine or an increase in homocysteine levels can lead to migraine attacks; therefore, vitamins could play a vital role in migraine prevention. For instance, riboflavin influences mitochondrial dysfunction and prevents migraine. Genes such as flavoenzyme 5,10-methylenetetrahydrofolate reductase (MTHFR), especially the C677T variant, have been associated with elevated plasma levels of homocysteine and migraine with aura. Homocysteine catalyzation requires the presence of vitamins B6, B12, and folic acid, which can decrease the severity of migraine with aura, making these vitamins potentially useful prophylactic agents for treating migraine with aura. Menstrual migraine, on the other hand, is associated with increased prostaglandin (PG) levels in the endometrium, indicating a role for vitamin E, which is an anti-PG. Vitamin C can also be used as a scavenger of reactive oxygen species for treating neurogenic inflammation in migraine patients. This paper reviews possible therapies based on vitamin supplementation for migraine prophylaxis, focusing on migraine with aura and menstrual migraine.

MicroRNAs (miRNAs) are short, endogenous, non-coding RNAs that post-transcriptionally regulate gene expression by base pairing with mRNA targets. Altered miRNA expression profiles have been observed in several diseases, including neurodegeneration. Multiple studies have reported altered expressions of miRNAs in the brains of individuals with Alzheimer’s disease (AD) as compared to those of healthy elderly adults. Some of the miRNAs found to be dysregulated in AD have been reported to correlate with neuropathological changes, including plaque and tangle accumulation, as well as altered expressions of species that are known to be involved in AD pathology. To examine the potentially pathogenic functions of several dysregulated miRNAs in AD, we review the current literature with a focus on the activities of ten miRNAs in biological pathways involved in AD pathogenesis. Comprehensive understandings of the expression profiles and activities of these miRNAs will illuminate their roles as potential therapeutic targets in AD brain and may lead to the discovery of breakthrough treatment strategies for AD.

Detection of markers for neurodegenerative disorders (NDDs) within brain tissue of Alzheimer’s disease (AD) or Parkinson’s disease (PD) patients has always been hampered by our inability to access tissue from living human subjects and obtain biopsy samples of key regions implicated in disease occurrence and progression. Currently, diagnosis of NDDs is principally based on clinical observation of symptoms that present at later stages of disease progression, followed by additional neuroimaging and, possibly, CSF evaluation. A way to potentially detect and diagnose NDDs at a far earlier stage is to screen for abnormal levels of specific disease markers within the peripheral circulation of patients with NDDs. Increasing evidence suggests that there is dysregulation of microRNAs (miRNAs) in NDDs. Peripheral blood mononuclear cells as well as biofluids, such as plasma, serum, urine and cerebrospinal fluid, contain miRNAs that can be identified and quantified. This opens the potential for circulating levels of miRNAs within blood or other biofluids to be characterized and used as a non-invasive diagnostic biomarker screen to support early disease detection and possible disease progression monitoring of NDDs such as AD and PD. Plainly, such a potential screen is only possible with a clear understanding of which miRNAs change with disease, and when this occurs during the progression of AD and PD. Such information is becoming increasingly available and in the near future may not only support disease diagnosis but provide the opportunity to evaluate therapeutic interventions earlier in the disease process where their targets may be more relevant to delay AD or PD progression.

Based on disability-adjusted life years, stroke is one of the major causes of death and is among the top five diseases in Nepal. Despite this fact, information on the prevalence, morbidity, and mortality of stroke in Nepal is limited to urban areas, with no official reports published on the epidemiology of stroke throughout the country. The mean age of stroke patients in Nepal is between 59 and 62 years, with males affected more frequently. Hypertension, cigarette smoking, alcohol consumption, and diabetes are the main predisposing factors for stroke, and ischemic stroke is more common (63%) than hemorrhagic stroke (37%). Because of a lack of facilities and specialists, most stroke patients, especially in the rural areas, seek traditional healers to treat their conditions. More governmental and non-governmental organizations should be involved in improving facilities and implementing prevention strategies.