Parkinson's disease: Research puts spotlight on thiamine deficiency and cardiovascular health.

The manuscript is a commenting on the article "Effects of vitamin B12, folate, and entacapone on homocysteine levels in levodopa-treated Parkinson's disease patients: A randomized controlled study", recently published by Anamnart and Kitjarak (2021), in this prestigious journal. The authors demonstrated that combination supplementation with vitamin B12 and folate was associated with significantly decreased plasma homocysteine (Hcy), suggesting that plasma Hcy levels should be monitored during levodopa treatment, and supplementation with inexpensive vitamin B12 and folate is beneficial for levodopa-treated PD patients. Considering some evidences - i) that it has to be indicated that dietary and supplemental thiamine intake has a protective effect on various medical conditions, including PD; ii) that several studies highlighted a possible relationship between PD low levels of thiamine in the serum, suggesting that elevated thiamine levels might protect against PD; iii) that thiamine deficiency is not just a common finding in patients with cardiovascular dysfunctions, but it might also have a role in the development and prognosis of PD - our research group believes that some comprehensive cardiovascular screening protocols should be developed for PD patients in order to reduce fatal events in these individuals.

Transcranial low-level laser therapy in an in vivo model of stroke: Relevance to the brain infarct, microglia activation and neuroinflammation.

Stroke is the main cause of death and functional disability. The available therapy affects only 5% of patients, and new therapeutic approaches have been constantly tested. Transcranial photobiomodulation (PBM) is promising for its neuroprotective effect on brain injuries. Thus, the present study investigated the PBM effects in an in vivo model of ischemic stroke induced by photothrombosis (PT). Five different groups of Wistar rats were submitted or not to a daily dose of fish oil or/and laser sessions for 2 months. The ischemia volume was evaluated by stereology; GFAP, Iba and NeuN by immunohistochemistry; TNF-α, IL-1ß, IL-6, IL-10 and TGF-ß by ELISA assay. PBM influenced both the lesion volume and the GFAP. Furthermore, PBM and Ω-3 or both reduced Iba RNAm. PBM reduced TNF-α, IL-1ß, IL-6, brain damage, neuroinflammation and microglial activation, and it increased astroglial activity in peri-lesioned region after stroke.

Fish oil provides protection against the oxidative stress in pilocarpine model of epilepsy.

Temporal lobe epilepsy (TLE), the most common form of epilepsy is often resistant to pharmacological treatment. Neuronal loss observed in epileptic brain may be result of an overproduction of free radicals (oxidative stress). Oxidative stress is characterized by an imbalance between antioxidant defenses and oxidizing agents (free radicals), which can lead to tissue injury. The n-3 PUFAs are important for the development and maintenance of central nervous system functions. Research by our group has shown that chronic treatment with fish oil, immediately after status epilepticus (SE), exhibits both neuroprotective effects and effects on neuroplasticity. The main purpose of this research was to evaluate if fish oil exhibits a protective effect against oxidative stress. Animals were subjected to TLE model by pilocarpine administration. After 3 h of SE they were randomly divided into the following groups: control animals treated daily with vehicle or with 85 mg/kg of fish oil and animals with epilepsy treated daily with vehicle or with 85 mg/kg of fish oil. After 90 days, superoxide anion production, enzymatic activity of superoxide dismutase (SOD) and catalase (CAT) and protein expression of NAD(P)H oxidase subunits (p47(PHOX) and gp91(PHOX)) were analyzed. Our results showed evidences that reactive oxygen species are increased in animals with epilepsy and that fish oil supplementation could counteract it. Fish oil supplementation promoted protection against oxidative stress by multiple ways, which involved the reduction of activity and expression of NAD(P)H oxidase subunits and increased the activity and expression of antioxidants enzymes, contributing to well-known neuroprotective effect in epilepsy.

Environmental air pollution is an aggravating event for sudden unexpected death in epilepsy.

It is extremely difficult to estimate the occurrence of sudden unexpected death in epilepsy (SUDEP). On the other hand, discovering and carefully evaluating new risk factors that may contribute to the onset of cardiovascular abnormalities in people with refractory epilepsy may prevent fatal events in these individuals. In this context, we should not ignore that urban air pollution is a leading problem for environmental health and is able to cause serious cardiovascular dysfunctions that culminate in sudden death. In this regard, we aimed to determine whether environmental exposure to air pollution is an aggravating event for SUDEP.