Current Neurovascular Research - Volume 22, Issue 2, 2025

An essential component of the endocannabinoid system, cannabinoid receptor type 1 (CB1) is primarily expressed in the central nervous system, where it regulates several neurophysiological activities. Neurotransmitter release, synaptic plasticity, mood modulation, and cognitive processes are all influenced by CB1 receptors. The CB1 receptor is closely linked to a wide range of brain-related disorders, and regulating its activity may be a way to treat several brain-related diseases.

Literature search across Google Scholar, Scopus, PubMed, and Web of Science, covering publications from 1985 to 2025, aimed to gather extensive information on the pharmacological role of the CB1 receptor in various brain illnesses. Using keywords such as “CB1,” “Brain,” “Epilepsy,” “Alzheimer’s,” “Parkinson’s disease,” “Neuroprotection,” and “Neurodegeneration,” this review consolidates existing knowledge and identifies potential avenues for future research.

This study incorporates pre-clinical evidence and highlights the involvement of the CB1 receptor in etiologies, symptoms, and treatments related to distinct brain-related disorders.

Potential treatment strategies that target the endocannabinoid system and the intricate relationship between CB1 receptor activity and its consequences in several brain disorders, including Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, depression, anxiety, etc., have been discussed. Additionally, the difficulties and disputes related to CB1 receptor modulation, including the contradictory actions of CB1 receptor agonists and antagonists, are also addressed.

The CB1 receptor is a promising therapeutic target for brain disorders due to its key role in regulating various physiological functions in the CNS, suggesting potential for the treatment of several brain disorders.

With 301 million cases worldwide, anxiety disorders represent a serious public health concern. Many people endure ongoing distress while receiving several treatments because of the drawbacks of traditional therapy, such as adverse effects, dependence, and inconsistent efficacy. This emphasizes the absolute need for novel treatment approaches.

This review examines emerging pharmacological and non-pharmacological strategies for anxiety disorders, assessing existing and developing therapeutic options while examining the drawbacks of conventional therapies.

A comprehensive literature review was carried out using the NIH, PubMed, and Google Scholar databases. Studies from 2020-2025 were given priority in the inclusion criteria, with a few supporting references from earlier years. Personalized medicine, combination therapy, non-pharmacological interventions, and novel anxiolytic targets, etc., were among the keywords used.

Conventional therapies, including benzodiazepines, SSRIs, and SNRIs, are still the major choices, but they have significant disadvantages. The protein kinase pathway, endocannabinoid and orexin systems, NK1R antagonists, and microbiome modulation are examples of emerging targets. Emerging strategies that show preliminary promise include digital therapeutics, gene therapy, optogenetics, personalized medicine, combination therapy, herbal therapy, and peptide-based medicines (e.g., NPY, NPS, oxytocin analogs, CRF, vasopressin, and melanocortin receptor antagonist). Several of these approaches modulate key neural circuits, such as the involvement of the amygdala–prefrontal cortex axis, via the HPA axis, and biomarker-informed personalization, among others; yet many remain in early-phase or preclinical investigation. However, limited comparative data exist between these novel strategies and standard therapies, underlining the need for rigorous head-to-head evaluations.

Advances in molecular neuroscience and precision medicine offer potential alternatives to conventional treatments. However, most emerging therapies require further clinical validation, large-scale trials, and translational refinement before they can be integrated into real-world decision-making for anxiety disorders.

Post-stroke dysphagia (PSD) is a common complication after acute stroke. It can be effectively alleviated by electroacupuncture (EA) stimulation at the Baihui acupoint; however, the underlying mechanism remains unclear.

Male ICR mice were used, and the suture occlusion method was employed to establish the middle cerebral artery occlusion (MCAO) mouse model. EA stimulation was applied to the Baihui acupoint for intervention. After treatment, the survival rate of the mice was assessed. Subsequently, a water swallow test was conducted to evaluate the degree of dysphagia in the mice. Additionally, neurological function was assessed through Garcia scoring and measurement of serum Ca²⁺-Mg²⁺-ATPase activity. Fur-thermore, MRI was utilized to evaluate the therapeutic effects of EA on cerebral infarction and edema rates. Then, the antioxidant activity of the EA intervention was assessed by measuring indicators of oxida-tive damage. Finally, the expressions of gamma-aminobutyric acid type B receptor subunit 1 (GAB-ABR1), N-methyl-D-aspartate receptor 1 (NMDAR1) were detected through WB, RT-qPCR, and immu-nofluorescence.

EA intervention effectively increased the survival rate of MCAO mice and alleviated their dysphagia. Additionally, the impaired neurological function of the mice was improved, and cerebral infarction and edema rates were reduced. Furthermore, EA alleviated oxidative stress in mice, reduced damage to neurons in the nucleus ambiguus, and upregulated GABABR1 while downregulating NMDAR1.

Although we suggested that EA may exert therapeutic activity for PSD by maintaining the balance of NMDAR1 and GABABR1, this conclusion still requires further experimental validation.

EA stimulation of the Baihui acupoint was effective in treating PSD, which was related to its ability to improve damaged neurons, upregulate GABABR1, and downregulate NMDAR1. These findings provided a new insight into the mechanisms of EA treatment for PSD and serve as a theoretical basis for future clinical research.

Current genetic research on the relationship between hypertension and vertigo is limited, and traditional observational studies cannot establish a causal relationship due to design limitations, particularly regarding whether hypertension acts as a causal risk factor for specific vertigo subtypes, such as benign paroxysmal positional vertigo (BPPV).

This study employed a two-sample MR approach to infer causal relationships via genome-wide association study (GWAS) data, thereby addressing the limitations of traditional observational studies. In addition to analyzing the link between total vertigo and hypertension, we examined three major types of vertigo: central vertigo, benign paroxysmal positional vertigo (BPPV), and other peripheral vertigo. The study included 3834 cases of BPPV, 186 cases of central vertigo, 1293 cases of other peripheral vertigo, and 209,582 controls. Various MR methods, including the inverse variance weighted (IVW) approach, MR-Egger, weighted median, and simple mode, were employed to deduce the potential causative associations.

A set of 53 genome-wide significant single-nucleotide polymorphisms (SNPs) associated with hypertension was identified as instrumental variables for subsequent MR analysis. The results indicated a significantly positive correlation between hypertension and the risk of total vertigo (OR: 1.16, 95% CI: 1.08-1.25, p <0.05), BPPV (OR: 1.12, CI: 1.01-1.24, and p =0.03), and other peripheral vertigo (OR: 1.19, 95% CI: 1.00-1.41, p =0.046), whereas no significant association was found with central vertigo (OR: 1.15, 95% CI: 0.74-1.80, p =0.53).

This study provides genetic evidence for a positive association between hypertension and vertigo, particularly BPPV and peripheral vertigo, but not central vertigo. Hypertension may induce vestibular dysfunction via vascular changes leading to tissue hypoxia and cochlear-vestibular degeneration. Limitations include small sample sizes for certain vertigo subtypes (e.g., central vertigo) and limited generalizability to non-European populations.

This MR analysis provides evidence supporting a potential causal relationship between hypertension and an increased risk of certain types of vertigo. These findings contribute to the understanding of risk factors and the early prediction of vertigo.

This study aimed to analyze the global, regional, and national burden and trends of stroke related to high consumption of processed meat from 1990 to 2021, using data from the Global Burden of Disease (GBD) Study 2021.

An observational trend analysis was conducted using data from the GBD Study 2021. Age-standardized rates for deaths and disability-adjusted life years (DALYs) were calculated using the world standard population. Estimated annual percentage change (EAPC) was assessed using linear regression models.

From 1990 to 2021, the global age-standardized death rate due to diet high processed meat-related stroke decreased from 0.80 per 100,000 (95% UI: 0.18 to 1.43) to 0.27 per 100,000 (95% UI: 0.06 to 0.46), with an EAPC of -4.23% (95% UI: -4.54 to -3.92). The age-standardized DALY rate also declined from 14.16 per 100,000 (95% UI: 3.19 to 25.49) to 5.20 per 100,000 (95% UI: 1.21 to 9.33), with an EAPC of -4.00% (95% UI: -4.34 to -3.67). Significant disparities were observed across regions and socioeconomic strata, with higher burdens in high-middle SDI regions. Females consistently had higher death and DALY rates and counts than males.

The study reveals a significant decline in both mortality and DALYs associated with a diet high in processed meat-related stroke over the three decades.

Our study highlighted the effectiveness of public health interventions. However, disparities persist across regions and socioeconomic strata, emphasizing the need for targeted and context-specific strategies to mitigate the burden of stroke related to high processed meat intake.

Anandamide (AEA), an endocannabinoid, has demonstrated analgesic and anti-inflammatory properties in various experimental models. However, the mechanisms underlying its role in neuropathic pain and inflammation remain unclear.

Carrageenan-induced inflammation and Chronic Constriction Injury (CCI) were used to model inflammatory and neuropathic pain in Wistar rats. Behavioral tests (e.g., paw edema, mechanical and thermal hyperalgesia), hematological and biochemical analyses, and molecular studies (mRNA expression of AEA pathway enzymes) were conducted to evaluate AEA’s therapeutic potential.

Anandamide significantly reduced paw edema and alleviated pain behaviors in CCI rats in a dose-dependent manner. It normalized hematological and biochemical markers and decreased levels of oxidative stress indicators (MDA, nitrite). mRNA analysis revealed upregulation of AEA degradation enzymes following CCI, indicating disrupted endocannabinoid signaling.

AEA’s analgesic and anti-inflammatory actions appear to be mediated through CB1 receptor activation and modulation of ATP-sensitive potassium channels. The observed improvements in biochemical and behavioral markers suggest its efficacy in modulating neuroinflammation and neuropathic pain.

Anandamide demonstrates significant potential as a therapeutic agent in managing neuropathic and inflammatory pain. Further studies are warranted to elucidate its mechanisms and optimize its clinical applicability.

High On-Treatment Platelet Reactivity (HTPR) is frequently observed after carotid endarterectomy (CEA) or stenting (CAS), but its association with adverse events remains uncertain. This systematic review and meta-analysis evaluate the association between HTPR and recurrent vascular events in these patients.

EMBASE, PubMed, and Cochrane Library were searched for eligible studies from inception to July 1, 2024. Two independent reviewers screened the records, extracted data, and assessed the bias using predefined criteria. A meta-analysis was conducted using RevMan 5.4 software. The primary outcome was the risk of recurrent ischemic events in patients with HTPR. Secondary outcomes included the risk of hemorrhage and carotid restenosis.

Eight studies involving 1,052 patients were included in the meta-analysis. This meta-analysis found that HTPR significantly increased the risk of adverse vascular events (OR = 2.41, 95% CI: 1.37-4.24), particularly in CAS patients (OR = 1.85, 95% CI: 1.14-2.98), but not in CEA patients (OR = 4.53, 95% CI: 0.52-39.12). Furthermore, HTPR was not significantly associated with an increased risk of bleeding (OR = 0.90, 95% CI: 0.24-3.37) or carotid restenosis (OR = 1.70, 95% CI: 0.38-7.55).

This meta-analysis demonstrates that HTPR may increase the risk of recurrent ischemic events in CAS patients, supporting the clinical utility of platelet function monitoring in this population. However, no significant association was observed between HTPR and hemorrhage or restenosis. These findings should be interpreted cautiously due to study limitations, including small sample sizes and heterogeneity in platelet function assessment methodologies. Large-scale prospective studies with standardized protocols are warranted to validate these observations.

HTPR may be associated with an increased risk of recurrent ischemic events in patients undergoing CAS, highlighting the potential value of platelet function monitoring.