The human central nervous system (CNS) has a limited capacity for regeneration and repair, as many other organs do. Partly as a result, neurological diseases are the leading cause of medical burden globally. Most neurological disorders cannot be cured, and primary treatments focus on managing their symptoms and slowing down their progression. Cell therapy for neurological disorders offers several therapeutic potentials and provides hope for many patients. Here we provide a general overview of cell therapy in neurological disorders such as Parkinson\'s disease (PD), Alzheimer\'s disease (AD), amyotrophic lateral sclerosis (ALS), Wilson\'s disease (WD), stroke and traumatic brain injury (TBI), involving many forms of stem cells, including embryonic stem cells and induced pluripotent stem cells. We also address the current concerns and perspectives for the future. Most studies for cell therapy in neurological diseases are in the pre-clinical stage, and there is still a great need for further research to translate neural replacement and regenerative therapies into clinical settings.

Traumatic brain injury (TBI) can cause disorders of consciousness (DOC) by impairing the neuronal circuits of the ascending reticular activating system (ARAS) structures, including the hypothalamus, which are responsible for the maintenance of the wakefulness and awareness. However, the effectiveness of drugs targeting ARAS activation is still inadequate, and novel therapeutic modalities are urgently needed.
The goal of this work is to describe the neural loops of wakefulness, and explain how these elements participate in DOC, with emphasis on the identification of potential new therapeutic options for DOC induced by TBI.
Hypothalamus has been identified as a sleep/wake center, and its anterior and posterior regions have diverse roles in the regulation of the sleep/wake function. In particular, the posterior hypothalamus (PH) possesses several types of neurons, including the orexin neurons in the lateral hypothalamus (LH) with widespread projections to other wakefulness-related regions of the brain. Orexins have been known to affect feeding and appetite, and recently their profound effect on sleep disorders and DOC has been identified. Orexin antagonists are used for the treatment of insomnia, and orexin agonists can be used for narcolepsy. Additionally, several studies demonstrated that the agonists of orexin might be effective in the treatment of DOC, providing novel therapeutic opportunities in this field.
The hypothalamic-centered orexin has been adopted as the point of entry into the system of consciousness control, and modulators of orexin signaling opened several therapeutic opportunities for the treatment of DOC.

BACKGROUND: This study aimed to re-establish a Population Pharmacokinetic (PPK) model of oral phenytoin to further optimize the individualized medication regimen based on our previous research.
METHODS: Patients with intracranial malignant tumor requiring craniotomy were prospectively enrolled according to the inclusion criteria. Genotypes of CYP2C9*1 or *3 and CYP2C19*1, *2 or *3 were determined by real time PCR (TaqMan probe) method. Serum concentrations of phenytoin on the 4th and 7th day after oral administration were determined using fluorescence polarization immunoassay. The PPK parameters were estimated using Nonlinear Mixed Effects Models (NONMEM) and internal validation was performed using bootstraps. The predictive performance of the final model was evaluated by Normalized Predictive Distribution Errors (NPDEs) and diagnostic goodness- of-fit plots.
RESULTS: A total of 390 serum samples were collected from 170 patients in PPK model building group. The population typical values for Vm, Km and the apparent volume of distribution (V) in the final model were 17.5 mg/h, 6.41 mg/L and 54.8 L, respectively. Internal validation by bootstraps showed that the final model was stable and reliable. NPDEs with a normal distribution and a scatterplot with symmetrical distribution showed that the final model had good predictive capability. Individualized dose regimens of additional 40 patients in the external validation group were designed by the present final PPK model. The percentages of patients with serum concentrations within the therapeutic range were 61.53% (24/39) on the 4th day and 94.87% (37/39) on the 7th day, which were higher than the 39.33% (59/150) and 52.10% (87/167) of above 170 patients (P < 0.0001).
CONCLUSIONS: The present PPK final model for oral phenytoin may be used to further optimize phenytoin individualized dose regimen to prevent early seizure in patients after brain injury if patient characteristics meet those of the population studied.

Traumatic brain injury (TBI) has turned into a major health and socioeconomic problem affecting young people and military personnel. Numerous TBI patients experienced the sequela of brain injury called cognitive impairment, which reduced functions in attention, working memory, motivation, and execution. In recent years, transcranial near-infrared laser therapy (tNiRLT) as a possible therapy has been gradually applied in treating cognitive impairment post-TBI. In the present review, the biological mechanisms of transcranial tNiRLT for TBI are synthesized mainly based on the photonic impact of chronic mild TBI. Various exciting molecular events possibly occur during the procedure, such as stimulation of ATP production, regional cerebral blood flow, acupoint, neurogenesis and synaptogenesis, as well as a reduction in anti-inflammatory effect. Some animal experiments and clinical studies of tNiRLT for TBI are outlined. Several labs have displayed that tNiRLT is effective not only in improving neurological functions but also in increasing memory and learning capacity in rodent animals\' model of TBI. In a 2 patients case report and a 11-case series, cognitive functions were ameliorated. Efficacy on cognitive and emotional effects was also observed in a double-blind, controlled clinical study. Several Randomized, parallel, double blind, sham-controlled trials are underway, aiming to evaluate the efficacy of tLED on cognitive functions and neuropsychiatric status in participants post-TBI. Therefore, tNiRLT is a promising method applied to cognitive impairment following TBI.

BACKGROUND: \"Shengyu\" decoction, a traditional Chinese medicine, has been used to treat diseases with deficit in \"qi\" and \"blood\" induced frequently by profound loss of blood or by long sores with heavy pus, in which a potential anti-inflammatory effect is implied. The modified \"Shengyu\" decoction (MSD) used in the present study was designed on the basis of the \"Shengyu\" decoction, additional four herbs were added in. Many ingredients in these herbs have been demonstrated to be anti-inflammatory and thus MSD may be used for the treatment of traumatic brain injury (TBI). To evaluate the neuroprotective effect and the underlying mechanisms of MSD on the rat brain after TBI.
METHODS: TBI was induced in the right cerebral cortex of male adult rats using Feeney\'s weight-drop method. The rats were administered a gavage of MSD (0.5, 1.0 or 2.0 ml/200 g) 6h after TBI. The neurological functions, brain water content, contusion volume, and neuron loss were determined. The levels of TNF-α, IL-1β, IL-6, and IL-10 and the number of GFAP- and Iba1-positive cells in the brain ipsilateral to TBI were also measured. Moreover, the influence of MSD on these variables was observed at the same time.
RESULTS: The neurological deficits, brain water content, and neuron loss were significantly reduced after 1.0 or 2.0 ml/200 g of MSD treatment but not after 0.5 ml/200 g. In addition, treatment with MSD (1.0 ml/200 g) significantly increased the level of IL-10 and reduced the level of TNF-α and IL-1β and the number of GFAP- and Iba1-positive cells after TBI. However, the contusion volume of brain tissue and the expression of IL-6 were not significantly changed.
CONCLUSIONS: MSD may be a potential therapeutic for the treatment of TBI because MSD alleviated secondary brain injury induced by TBI. In addition, MSD inhibited the inflammatory response through reducing the expression of inflammatory cytokines and the activation of microglial cells and astrocytes in the brain tissue of rats after TBI. Therefore, a potential anti-inflammatory mechanism of the \"Shengyu\" decoction was confirmed, which may be one of the main reasons of \"Shengyu\" decoction used to treat diseases with obvious inflammatory responses.