Volume 28, Issue 7

Depression is a prevalent devastating mental disorder that affects the normal life of patients and brings a heavy burden to whole society. Although many efforts have been made to attenuate depressive/anxiety symptoms, the current clinic antidepressants have limited effects. Scientists have long been making attempts to find some new strategies that can be applied as the alternative antidepressant therapy. Exercise, a widely recognized healthy lifestyle, has been suggested as a therapy that can relieve psychiatric stress. However, how exercise improves the brain functions and reaches the antidepressant target needs systematic summarization due to the complexity and heterogeneous feature of depression. Brain plasticity, especially adult neurogenesis in the hippocampus, is an important neurophysiology to facilitate animals for neurogenesis can occur in not only humans. Many studies indicated that an appropriate level of exercise can promote neurogenesis in the adult brains. In this article, we provide information about the antidepressant effects of exercise and its implications in adult neurogenesis. From the neurogenesis perspective, we summarize evidence about the effects of exercise in enhancing neurogenesis in the hippocampus through regulating growth factors, neurotrophins, neurotransmitters and metabolism as well as inflammations. Taken together, a large number of published works indicate the multiple benefits of exercise in the brain functions of animals, particularly brain plasticity like neurogenesis and synaptogenesis. Therefore, a new treatment method for depression therapy can be developed by regulating the exercise activity.

There are many factors that strongly influence the aetiology, development, and progression of cognitive decline in old age, mild cognitive impairment (MCI), and Alzheimer’s disease (AD). These factors include not only different personality traits and moods but also lifestyle patterns (e.g. exercise and diet) and awareness levels that lead to cognitive decline in old age. In this review, we discuss how personality traits, mood states, and lifestyle impact brain and behaviour in older adults. Specifically, our review shows that these lifestyle and personality factors affect several brain regions, including the hippocampus, a region key for memory that is affected by cognitive decline in old age as well as AD. Accordingly, appropriate recommendations are presented in this review to assist individuals in decreasing chances of MCI, dementia, AD, and associated symptoms.

Type 2 diabetes mellitus (T2DM) is a global epidemic disease and has become a significant health problem. Many studies have raised concern about the mild cognitive impairment (MCI) with T2DM and even the Alzheimer’s disease patients with T2DM. The incidence of MCI is higher in individuals with T2DM than those without diabetes. Cognitive changes might affect everyday activities depending on the work and situation. Although the exact pathophysiology of MCI in T2DM is unclear, many studies suggest that the alterations in pathoglycemia, diabetic complications, related end products, and physical/psychological status are significant risk factors. In this article, we systematically overview the studies to illustrate the related risk factors of cognitive impairment in patients with T2DM. Further high quality studies and treatment need to be initiated and it will become incumbent on clinicians to identify and cure the earliest signs of clinical impairment.

Recent clinical trials of mesenchymal stem cells (MSCs) transplantation have demonstrated procedural safety and clinical proof of principle with a modest indication of benefit in patients with amyotrophic lateral sclerosis (ALS). While replacement therapy remained unrealistic, the clinical efficacy of this therapeutic option could be potentially enhanced if we could better decipher the mechanisms underlying some of the beneficial effects of transplanted cells, and work toward augmenting or combining these in a strategic manner. Novel ways whereby MSCs could act in modifying disease progression should also be explored. In this review, I discuss the known, emerging and postulated mechanisms of action underlying effects that transplanted MSCs may exert to promote motor neuron survival and/or to encourage regeneration in ALS. I shall also speculate on how transplanted cells may alter the diseased environment so as to minimize non-neuron cell autonomous damages by immune cells and astrocytes.

Major depressive disorder (MDD) and bipolar disorder (BD) are among the leading causes of burden and disability worldwide. Despite intensified research efforts to improve the treatment options and remission rates in mood disorders, no disease modifying treatment exists for these disorders. Accumulating evidence implicates the involvement of the gut microbiota in processes relevant to etiopathology of central nervous system-based disorders. The objective of this article was to critically evaluate the evidence supporting the link between gastrointestinal microbiota and mood disorders and to discuss the potential benefits of using probiotics in the treatment of MDD and BD. The concept of psychobiotics, which is bacterial-based interventions with mental health benefit, is emerging in the field. On the other hand, while probiotics might potentially represent a significant advance, specific roles of microbiota in the pathophysiology of mood disorders still need further investigation along with intervention studies.

No satisfactory effective therapy is still available to treat trauma- or disease-induced neuropathic pain, and current available treatment options have several side effects. Pulsed magnetic field (PMF) treatments are receiving growing interest as a therapeutic approach for several neuronal diseases. Although the exact mechanism of action of PMF treatments is unknown, reported findings represent a promising alternative therapeutic choice for the management of neuropathic pain. PMF treatments can supply new strategies for the therapy of life-threatening neuropathic pain due to its antihyperglycemic, anti-inflammatory, antihyperalgesic, antiallodynic, and neuroimmunomodulatory actions. In this review, I summarized the several recent findings about antineuropathic actions of PMF treatment in experimental animals with neuropathic pain induced by disease and/or damage.

Mast cells are immunological cells that are diversely distributed in different parts of the body. Their role in various pathological conditions such as hypersensitivity, atherosclerosis, pulmonary hypertension, and male infertility has been reported by different scientists. Apart from these, a number of studies have shown their important role in pathogenesis of neuropathic pain of diverse aetiology. They have been found to release active mediators, primarily histamine and serotonin on degranulation in response to different stimuli including chemical, nerve damage, toxin or disease-related conditions. The mast cells stabilizer has shown pain attenuating effects by preventing degranulation of mast cells. Similarly, compound 48/80 (first dose 200 μg/100 g and after 6-h interval, second dose of 500 μg/100 g) caused the degranulation of the accumulated endoneurial histamine and 5-HT antagonists have shown pain relieving effects by attenuating the effects of histamine and serotonin, respectively. On the other hand, the mast cell degranulator compound 48/80 has shown dual action depending on its time of administration. The present review discusses the critical role of mast cells in the generation and maintenance of neuropathic pain in experimental models.

Brain ageing is a complex process which in its pathologic form is associated with learning and memory dysfunction or cognitive impairment. During ageing, changes in cholinergic innervations and reduced acetylcholinergic tonus may trigger a series of molecular pathways participating in oxidative stress, excitotoxicity, amyloid-β toxicity, apoptosis, neuroinflammation, and perturb neurotrophic factors in the brain. Nicotine is an exogenous agonist of nicotinic acetylcholine receptors (nAChRs) and acts as a pharmacological chaperone in the regulation of nAChR expression, potentially intervening in age-related changes in diverse molecular pathways leading to pathology. Although nicotine has therapeutic potential, paradoxical effects have been reported, possibly due to its inverted U-shape dose-response effects or pharmacokinetic factors. Additionally, nicotine administration should result in optimum therapeutic effects without imparting abuse potential or toxicity. Overall, this review aims to compile the previous and most recent data on nicotine and its effects on cognition-related mechanisms and age-related cognitive impairment.

Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disorder that imposes heavy financial burden on governments and families of affected children. It is considered a multifactorial condition, where trace elements are among environmental factors that may contribute to ASD. Meanwhile, the between-study variance is high. The present systematic review was designed to investigate the difference in trace element measures between patients with ASD and control subjects. Meta-analyses showed that the hair concentrations of chromium ( p =0.024), cobalt ( p =0.012), iodine ( p =0.000), iron ( p =0.017), and magnesium ( p =0.007) in ASD patients were significantly lower than those of control subjects, while there were higher magnesium levels in the hair of ASD patients compared to that of controls ( p =0.010). Patients with ASD had higher blood levels of copper ( p =0.000) and lower levels of zinc compared to controls ( p =0.021). Further urinary iodine levels in patients with ASD were decreased in comparison with controls ( p =0.026). Sensitivity analyses showed that ASD patients in non-Asian but not in Asian countries had lower hair concentrations of chromium compared to controls. Also, such analyses indicated that ASD patients in Asian countries had lower hair zinc concentrations, whereas ASD patients in non-Asian countries had higher hair zinc concentrations in comparison with control subjects. This study found significant differences in the content of trace elements between patients with ASD compared to controls. The findings help highlighting the role of trace elements as environmental factors in the etiology of ASD.

In this review, we provide an overview of the relationship between cannabis use and the development of schizophrenia, using both animal and human studies. We further discuss the potential neural mechanism that may mediate the relationship between cannabis use and schizophrenia symptoms. We finally provide clinical implications and future studies that can further elucidate the relationship between cannabis and schizophrenia.