The neurological disorder known as Progressive Supranuclear Palsy, or PSP, is characterized by severe difficulties in movement and balance, which frequently result in falls and a decrease in function. Sensory cueing techniques such as Auditory Stimulation and visual stimulation that utilizes external cues to enhance motor coordination and gait performance in movement disorders. Sixty people with a diagnosis of progressive supranuclear palsy (PSP) were chosen by convenience sampling and split up into two groups: thirty in the experimental group received balance exercises and rhythmic auditory stimulation, while thirty in the control group received balance training and visual cueing. Over a six-week period, both therapies were given for 40 minutes, five days a week. Before and after the intervention, gait performance was evaluated using the 10-Meter Walk Test and the Timed Up and Go (TUG) Test. The Timed Up and Go (TUG) Test and the 10-Meter Walk Test showed statistically significant improvements in the Rhythmic Auditory Stimulation (RAS) group as compared to the visual cueing group (P-value <0.0001). By encouraging better health outcomes through non-invasive rehabilitation, this research supports good health and well-being. It also reduces inequality by ensuring that people with neurodegenerative illnesses have fair access to effective rehabilitation. In conclusion, rhythmic auditory stimulation significantly improves gait speed and motility in individuals with progressive supranuclear palsy (PSP) when paired with balance training.

Recently, in the field of neuroengineering, the Action Potential Generator (APG) is an essential component used to stimulate electrical impulses during communication among neurons. Besides, the generators are required in various applications, such as neural prosthetics, brain-computer interfaces, and neuronal behavioural studies. However, traditional methods for APG in electrical neurons often rely on intricate biological systems or complex electronic circuits, which can limit efficacy and flexibility in real-time environments. In addition, these techniques can be limited in scalability, consume high power, and present issues when combined with existing neural interfaces. As a result, the proposed design creates an efficient, flexible system by combining cutting-edge materials with flexible parts. The main advancement is the combination of flexible parts and cutting-edge materials to produce a physical action potential generator with highly biomimetic and adjustable outputs. By offering previously unheard-of control and fidelity in simulating natural neural activity for research and development, particularly as a tissue-free platform for electrode testing, the generator enables a vast array of firing patterns comparable to those of biological neurons, greatly improving the reliability of neural signal transmission. Hence, the proposed APG represents a substantial advance in neuroengineering and provides a versatile and effective solution for generating electrical signals in neurons.

Alzheimer's disease is a neurodegenerative disease characterized by an accumulation of amyloid beta peptide and hyperphosphorylation of Tau protein, as well as alterations in lipids that are important components of cell membranes. However, the mechanism of phospholipids in AD is not yet fully understood. This mini-review aims to explore the role of phospholipid biomarkers in the diagnosis, prognosis, and progression of the disease. A search was performed in several databases, including PubMed, PubMed Central, and ScienceDirect, with keywords such as "phospholipid biomarkers," "Alzheimer," and "non-sporadic diagnosis." A total of 30 articles were found, in which we discovered that phospholipid species such as ceramides, sphingomyelins, phosphatidylcholines, lysophosphatidylcholines, ethanolamine plasmalogens, phosphatidylethanolamines, and 2-aminoethyl dihydrogen phosphate were altered, showing that plasma lipids can be used as biomarkers for the diagnosis of AD, as well as to predict the prognosis and classify the severity of the disease. Nevertheless, although the findings are promising, further clinical validation through larger, more extensive studies is still required to consolidate their diagnostic and prognostic applications.

The involvement of high-frequency brainwaves in the neural processing of rhythmic Quranic recitation remains unclear, compared to the low-frequency brainwaves. This study examined the synchronisation of high-frequency gamma brainwaves (30–80 Hz) during passive listening to Quranic recitation in three different rhythmic styles. This experimental, cross-sectional study involving 29 healthy adult participants (14 Muslim, 15 non-Muslim) was conducted at the MEG laboratory at Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia. The average gamma source estimation was calculated using minimum-norm imaging, and the whole-brain functional connectivity of magnetoencephalography-electroencephalography (M/EEG) data was quantified using phase-locking value. The results revealed that the gamma waves synchronised in a network of brain regions that included the supramarginal gyrus, anterior cingulate cortex, hippocampus, central region, temporal lobe, inferior frontal gyrus, Rolandic and frontal operculum, cerebellum, visual network regions, and superior parietal gyrus. The findings highlight brain-wide activation during Quranic recitation in Quran-naïve non-Muslim participants, comparable to that in Muslim participants familiar with the employed rhythmic recitation. Both groups also exhibited increased language perception of the Quranic recitation, although they did not understand Arabic (non-Arab natives). The high-frequency gamma activity in this study suggests that receptive listening to different styles of rhythmic Quranic recitation engages neural networks responsible for language and musical perception, emotional regulation, memory and attention, visual mental imagery, and multisensory processing.

Consequences of chronic ethanol exposure on cognitive and motor functions are widely studied due to the neurodegeneration that ethanol produces in the cerebellum and other brain areas, including some corticolimbic regions. However, there is scarce information about the structural neuroplasticity effects of chronic ethanol exposure that ultimately lead to characteristic neurodegenerative consequences. For this purpose, we evaluated the effects of chronic ethanol exposure in adult male rats on exploratory behavior (locomotor activity induced by a novel environment) and structural neuroplasticity in corticolimbic and cerebellar neurons. After 90 days of ad libitum ethanol (10%) exposure, the locomotor behavior of the animals did not differ from that of the control group (exposed to water). Structural neuroplasticity was assessed using the Golgi-Cox technique in neurons from corticolimbic areas and the cerebellum. The findings revealed that ethanol exposure induced basilar dendritic atrophy without modifying the dendritic spine density in pyramidal cells in prefrontal cortex layers 3 and 5, the CA1 region of the dorsal hippocampus, and the basolateral amygdala. In contrast, ethanol exposure hypotrophied the dendritic arbor of Purkinje cells and reduced the density of dendritic spines in these cells. These data contribute to the knowledge of the neuroplasticity-related mechanisms underlying the neurodegenerative consequences of chronic ethanol exposure and its cognitive implications.

Tuberculous radiculomyelitis (TBRM) is a rare complication of tuberculosis which affects the nervous system. Common symptoms associated with TBRM include paraparesis or quadriparesis, urinary retention or constipation, and paraesthesia in the lower extremities. The ascending symptoms are often described as similar to Guillain Barre syndrome. A 21-year-old woman experienced progressive weakness from her lower to upper extremities, which eventually led to complete immobility within two days and was accompanied by autonomic dysfunction. Lumbar puncture demonstrated yellow and clear cerebrospinal fluid (CSF) with pleocytosis (214 cells/uL), neutrophil predominance (81%), increased protein (429mg/dL), and decreased CSF/serum glucose ratio (7 mg/dL vs. 159.3 mg/dL). Cervicothoracic MRI examination revealed multifocal hyperintense lesions with indistinct borders at the T5-T12 level and central predominance. These results indicate tuberculosis as the aetiology. This case illustrates the atypical manifestations of TB within the nervous system. In highly endemic countries like Indonesia, TB should be considered as one of the potential causes in the differential diagnosis of any progressive weakness involving the nervous system. The limited availability of high-sensitivity diagnostic tests for detecting Mycobacterium tuberculosis in the central nervous system remains a significant challenge.

Stroke remains a significant global cause of death and long-term disability, categorized into hemorrhagic stroke, ischemic stroke, and transient ischemic attack. Recovery outcomes can vary greatly, often influenced by genetic factors. This review highlights key genes involved in stroke recovery, including brain-derived neurotrophic factor (BDNF), glial cell-derived neurotrophic factor (GDNF), insulin-like growth factor-1 (IGF-1), vascular endothelial growth factor (VEGF), C-X-C motif chemokine ligand 12 (CXCL12), hypoxia-inducible factor 1-alpha (HIF1A), nuclear factor erythroid 2-related factor 2 (NRF2), nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 (NLRP3), sirtuin 1 (SIRT1), and tissue inhibitor of metalloproteinase 3 (TIMP3). These genes play important roles in neurotrophic support and neuronal survival, angiogenesis, inflammation and immune modulation, and extracellular matrix remodeling after stroke. Insights from both human and animal studies underscore the potential of these genetic markers as prognostic indicators and therapeutic targets for stroke recovery. Understanding these factors may lead to more personalized rehabilitation strategies, and future research is needed to explore gene-environment interactions and translate genetic findings into effective stroke recovery therapies.

Functional Cognitive Disorder (FCD) is a subtype of Functional Neurological Disorder (FND), with diagnostic criteria that have only recently been established in a major disease classification system. Although objective neuropsychological measures are not required for diagnosing FCD, they can provide valuable insights into discrepancies between subjective cognitive complaints, functionality, and objective neuropsychological performance. We present the case of a 51-year-old Malay female with a history of Major Depressive Disorder who developed neurocognitive complaints affecting her occupational and social functioning following the sudden death of her husband. A comprehensive assessment, including neuropsychological testing, brain MRI, and laboratory investigations, was conducted. Neuropsychological evaluation revealed significant impairments across multiple neurocognitive domains. However, the presence of situational and mood-related variability in memory performance, along with an inconsistency between the severity of her objective cognitive impairments and her largely preserved ability to perform instrumental activities of daily living (IADLs), supported a diagnosis of FCD. The diagnosis and management of FCD require a multidisciplinary approach. Clinical neuropsychology plays a crucial role in both diagnosing and understanding FCD by assessing neurocognitive functioning and intrapsychic processes. The use of various psychological instruments can help elucidate the neurocognitive profile of FCD to inform a more comprehensive and individualized management plan.