Cerebrovascular disease is uncommon in patients with HIV, occurring in up to 1.9% of patients, 0.2% were presenting with transient ischemic attacks. The central nervous system is the first part of the body to be affected by the human immunodeficiency virus. This case report is a unique presentation of a 33-year-old male who presented with focal neurologic deficits that lasted for one hour with a background of promiscuous history. The patient was positive for HIV screening test and CD4 count and was started on a combination of antiretroviral therapy. This is the first documented case report in the Philippines. This case report demonstrates the need for a high index of suspicion for early detection of the cause in HIV-positive patients with recurrent transient ischemic attacks, given the high morbidity and mortality that is associated with this condition if delayed or undiagnosed.

OBJECTIVE

To evaluate cone- and rod-specific nonperfusion indices (CPI, RPI) on ultrawide field fluorescein angiography (UWF-FA) and their correlation with diabetic retinopathy (DR) severity and center-involving diabetic macular edema (ciDME).

Sixty-nine eyes of 43 patients with diabetes underwent UWF color photography (UWF-CP), UWF-FA, and macular optical coherence tomography (OCT). DR severity was graded by a masked reader on UWF-CP. UWFFA images were segmented into posterior pole (≤10 mm from fovea), mid-periphery (10–15 mm) and far periphery (>15 mm), and into the macula, within ETDRS fields and extended peripheral fields. Ischemic areas were quantified using ImageJ to calculate nonperfusion index (NPI), CPI, and RPI. ciDME was determined on OCT. Correlations were analyzed using Pearson coefficients (r).

DR severity correlated significantly with global NPI (r = 0.56, p < 0.0001) and across all retinal zones (r = 0.35– 0.57). Both CPI (global: r = 0.56, p < 0.0001; zones: r = 0.42–0.59) and RPI (global: r = 0.55, p < 0.0001; zones: r = 0.40–0.59) showed similar associations. ciDME presence was also correlated with NPI (global: r = 0.40, p = 0.0014; zones: r = 0.42–0.54), CPI (global: r = 0.47, p = 0.0001; zones: r = 0.32–0.55), and RPI (global: r = 0.46, p = 0.0002; zones: r = 0.33–0.54).

Cone- and rod-related retinal nonperfusion strongly correlate with DR severity and ciDME. UWF-FA may help identify high-risk eyes and guide surveillance of ischemia-related progression. Further studies are needed to define ischemic thresholds predictive of vision-threatening complications.

OBJECTIVE: To elucidate the modulation mechanism of Suanzaoren Decoction (SZRD) on basolateral amygdala (BLA) neuronal activity to alleviate chronic restraint stress (CRS)-related behavioral deficits. METHODS: The male C57BL/6J mice were assigned to 4 groups using the complete randomization method, including control (CON, n=19), CRS (n=19), SZRD (n=21), and fluoxetine (Flu, n=22) groups. Mice were restrained for 6 h per day, over a 21-d period to establish CRS models. The CON group remained in their cages without food or water during the 6-h matching period. SZRD and Flu groups received intragastric administration of SZRD (4.68 g/kg) and Flu (20 mg/kg) daily, respectively, 30 min before restraint for 21 consecutive days. The therapeutic effects of SZRD were evaluated using behavioral tests including the tail suspension test, elevated plus maze test, and forced swimming test. The cellular Fletcher B. Judson murine osteosarcoma proto-oncogene (c-Fos) expression in the BLA was measured using immunofluorescence, while action potential (AP) firing and synaptic transmission in BLA pyramidal neurons were evaluated using whole-cell patch-clamp recordings. RESULTS: SZRD administration significantly increased time spent in the open arms and open-arm entries while reducing immobility time (P<0.05 or P<0.01). It downregulated CRS-induced c-Fos expression and AP firing of pyramidal neurons in the BLA (P<0.01). Additionally, SZRD selectively attenuated excitatory (P<0.01), but not inhibitory, synaptic transmission onto BLA pyramidal neurons. CONCLUSION SZRD alleviated CRS-induced anxiety- and depression-like behaviors in mice by modulating the excitability and synaptic transmission of BLA pyramidal neurons.
Animals ; Drugs, Chinese Herbal/therapeutic use* ; Depression/complications* ; Pyramidal Cells/pathology* ; Male ; Mice, Inbred C57BL ; Basolateral Nuclear Complex/pathology* ; Restraint, Physical ; Anxiety/complications* ; Behavior, Animal/drug effects* ; Stress, Psychological/physiopathology* ; Mice ; Proto-Oncogene Proteins c-fos/metabolism* ; Action Potentials/drug effects* ; Synaptic Transmission/drug effects*

Chronic pain, a prevalent chronic disease, frequently manifests not only in physical symptoms but also in cognitive impairment, which seriously affects patients' quality of life. Interneurons are multipolar neurons, most of which are inhibitory, serving as crucial connectors within neural networks. They play key roles in signal transmission and fine-tuning of neural activity. In recent years, growing evidence has shown that interneurons are involved in the development of chronic pain and its associated cognitive dysfunction. Investigating the relationship between interneuron dysfunction and chronic pain-related cognitive impairment is of great significance, offering new potential targets and insights for the development of novel therapeutic approaches.
Interneurons/physiology* ; Humans ; Chronic Pain/complications* ; Cognitive Dysfunction/physiopathology* ; Cognition Disorders/physiopathology* ; Animals

Myelin formation is considered the last true "invention" in the evolution of vertebrate nervous system cell structure. The rapid jumping pulse propagation achieved by myelin enables the high conduction speed that is the basis of human movement, sensation, and cognitive function. As a key structure in the brain, white matter is the gathering place of myelin. However, with age, white matter-associated functions become abnormal and a large number of myelin sheaths undergo degenerative changes, causing serious neurological and cognitive disorders. Despite the extensive time and effort invested in exploring myelination and its functions, numerous unresolved issues and challenges persist. In-depth exploration of the functional role of myelin may bring new inspiration for the treatment of central nervous system (CNS) diseases and even mental illnesses. In this study, we conducted a comprehensive examination of the structure and key molecules of the myelin in the CNS, delving into its formation process. Specifically, we propose a new hypothesis regarding the source of power for myelin expansion in which membrane compaction may serve as a driving force for myelin extension. The implications of this hypothesis could provide valuable insights into the pathophysiology of diseases involving myelin malfunction and open new avenues for therapeutic intervention in myelin-related disorders.
Myelin Sheath/metabolism* ; Humans ; Central Nervous System/metabolism* ; Animals

Abuse of amphetamine-based stimulants is a primary public health concern. Recent studies have underscored a troubling escalation in the inappropriate use of prescription amphetamine-based stimulants. However, the neurophysiological mechanisms underlying the impact of acute methamphetamine exposure (AME) on sleep homeostasis remain to be explored. This study employed non-human primates and electroencephalogram (EEG) sleep staging to evaluate the influence of AME on neural oscillations. The primary focus was on alterations in spindles, delta oscillations, and slow oscillations (SOs) and their interactions as conduits through which AME influences sleep stability. AME predominantly diminishes sleep-spindle waves in the non-rapid eye movement 2 (NREM2) stage, and impacts SOs and delta waves differentially. Furthermore, the competitive relationships between SO/delta waves nesting with sleep spindles were selectively strengthened by methamphetamine. Complexity analysis also revealed that the SO-nested spindles had lost their ability to maintain sleep depth and stability. In summary, this finding could be one of the intrinsic electrophysiological mechanisms by which AME disrupted sleep homeostasis.
Animals ; Methamphetamine ; Electroencephalography ; Male ; Sleep/drug effects* ; Central Nervous System Stimulants ; Delta Rhythm/drug effects* ; Sleep Stages/drug effects*

OBJECTIVES: To investigate the mechanism by which the pyramidal neurons of the anterior cingulate cortex (ACC) modulate the effects of enriched environment (EE) for relieving anxiety-like behaviors in mice. METHODS: C57BL/6J mice were randomly divided into control group, restraint stress (RS) group, and RS+EE group (n=8). The mice in the latter two groups were subjected to RS for 2 h daily for 3 days, and those in RS+EE group were housed in an EE during modeling. Anxiety-like behaviors of the mice were evaluated using the elevated plus-maze tests (EPM) and open field test (OFT). Changes in c-Fos expression in the ACC of the mice were detected with immunofluorescence assay, and pyramidal neuron excitability in the ACC (Pyn^ACC) was measured using patch-clamp technique. The miniature excitatory and inhibitory postsynaptic currents (mEPSC and mIPSC, respectively) were analyzed to assess synaptic transmission changes. RESULTS: Behavioral tests showed obvious anxiety-like behaviors in RS mice, and such behavioral changes were significantly improved in RS+EE mice. Immunofluorescence staining revealed significantly increased c-Fos expression in the ACC in RS mice but lowered c-Fos expression in RS+EE group. Compared with the control mice, the RS mice showed increased action potential firing rate of Pyn^ACC, which was significantly reduced in RS+EE group. Compared with the RS mice, the RS+EE mice showed also decreased frequency of mEPSCs of Pyn^ACC, but the amplitude exhibited no significant changes. No obvious changes in the frequency or amplitude of mIPSCs were observed in RS+EE mice. CONCLUSIONS EE reduces excitability of Pyn^ACC to alleviate anxiety-like behaviors induced by RS in mice.
Animals ; Anxiety/physiopathology* ; Gyrus Cinguli ; Mice, Inbred C57BL ; Mice ; Pyramidal Cells/physiology* ; Restraint, Physical ; Stress, Psychological ; Proto-Oncogene Proteins c-fos/metabolism* ; Male ; Behavior, Animal ; Environment ; Excitatory Postsynaptic Potentials

Extracellular vesicles (EVs), nanoscale lipid bilayer vesicles actively secreted by organisms into the extracellular environment, are rich in specific bioactive substances, such as proteins, genetic materials and lipids. These vesicles are involved in intercellular interactions and can pass through the blood-brain barrier, and may thus potentially serve as important biological substances for treatment of neurological diseases. In this review, we summarize the biological origin of EVs and their therapeutic potential in neurological diseases, expound the possibility of EV-based treatment of neurological diseases using traditional Chinese medicine, and discuss the challenges and prospects of researches of EVs for the treating neurological diseases.
Extracellular Vesicles ; Humans ; Nervous System Diseases/therapy* ; Medicine, Chinese Traditional

The nervous system is the dominant regulatory system in the human body. The traditional theory is that tumors lack innervation. However, an increasing number of studies have shown complex bidirectional interactions between tumors and the nervous system. Globally, colorectal cancer (CRC) is the third most common cancer. With the rise of tumor neuroscience, the role of nervous system imbalances in the occurrence and development of CRC has attracted increasing amounts of attention. However, there are still many gaps in the research on the interactions and mechanisms involved in the nervous system in CRC. This article systematically reviews emerging research on the bidirectional relationships between the nervous system and CRC, focusing on the following areas: (1) Effects of the nervous system on colon cancer. (2) Effects of CRC on the nervous system. (3) Treatment of CRC associated with the nervous system.
Humans ; Colorectal Neoplasms/therapy* ; Animals ; Nervous System/metabolism*

In the mammalian central nervous system (CNS), astrocytes are the ubiquitous glial cells that have complex morphological and molecular characteristics. These fascinating cells play essential neurosupportive and homeostatic roles in the healthy CNS and undergo morphological, molecular, and functional changes to adopt so-called 'reactive' states in response to CNS injury or disease. In recent years, interest in astrocyte research has increased dramatically and some new biological features and roles of astrocytes in physiological and pathological conditions have been discovered thanks to technological advances. Here, we will review and discuss the well-established and emerging astroglial biology and functions, with emphasis on their potential as therapeutic targets for CNS injury, including traumatic and ischemic injury. This review article will highlight the importance of astrocytes in the neuropathological process and repair of CNS injury.
Astrocytes/drug effects* ; Humans ; Animals ; Central Nervous System/pathology* ; Central Nervous System Diseases/physiopathology*