Neuroscience
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Transient receptor vanillin 1 (TRPV1) is widely expressed in the neural axis and surrounding tissues, and is easily activated by harmful stimuli such as pain and inflammatory responses. Previous studies have shown that activated TRPV1 channels regulate all levels of nervous system activity by improving calcium influx and modulating nervous system excitability. Recent studies have suggested that TRPV1 activation in the peripheral nervous system may induce sleep disorders, while activation in the central nervous system may ameliorate sleep disorders and assist memory consolidation processes. Here, we summarize the risk factors for inducing sleep disorders, the alteration of these risk factors by TRPV1 receptor activation, and the driving effect of TRPV1 receptor activity on memory consolidation.
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Parkinson's disease (PD) is a prevalent neurodegenerative disorder caused by degeneration of dopaminergic neurons, originating from the substantia nigra pars compacta, and characterized by motor symptoms such as bradykinesia, muscle rigidity, resting tremor, and postural instability, as well as non-motor symptoms such as anxiety, depression, reduced sense of smell, cognitive impairment, and visual dysfunction. Emerging evidence highlights the retina as a promising site for non-invasive exploration of PD pathology, due to its shared embryonic origin with the central nervous system. ⋯ This review provides a comprehensive synthesis of retinal dysfunctions in PD, focusing on structural and functional changes as potential biomarkers for early diagnosis and clinical assessment. By integrating findings from advanced imaging and electrophysiological studies, this review introduces novel perspectives on the correlation between retinal changes and PD pathophysiology, offering innovative approaches for early detection, disease progression monitoring, and therapeutic stratification.
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Neurodegenerative diseases (ND) are complex diseases of still unknown etiology. Lately, long non-coding RNAs (lncRNAs) have become increasingly popular and implicated in several pathologies as they have several roles and appear to be involved in all biological processes such as cell signaling and cycle control as well as translation and transcription. MEG3 is one of these and acts by binding proteins or directly or competitively binding miRNAs. ⋯ This review examines the current state of knowledge concerning the level of expression and the regulatory function of MEG3 in relation to several NDs. In addition, we examined the relation of MEG3 with neurotrophic factors such as Tumor growth factor β (TGFβ) and its possible mechanism of action. A comprehensive and in-depth analysis of the role of MEG3 in ND could give a clearer picture about the initiation of the process of neuronal death and help develop an alternative therapy that targets MEG3.
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Review
Emerging biophysical techniques for probing synaptic transmission in neurodegenerative disorders.
Plethora of research has shed light on the critical role of synaptic dysfunction in various neurodegenerative disorders (NDDs), including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD). Synapses, the fundamental units for neural communication in the brain, are highly vulnerable to pathological conditions and are central to the progression of neurological diseases. The presynaptic terminal, a key component of synapses responsible for neurotransmitter release and synaptic communication, undergoes structural and functional alterations in these disorders. ⋯ The review articles highlighted provide a comprehensive overview of how synaptic vulnerability and pathology are shared mechanisms across a spectrum of neurological disorders. In major neurodegenerative diseases, synaptic dysfunction is a common thread linking these conditions. The intricate molecular machinery involved in neurotransmitter release, synaptic vesicle dynamics, and presynaptic protein regulation are key areas of focus for understanding synaptic alterations in neurodegenerative diseases.
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This study assessed the neural mechanisms and relative saliency of categorization for speech sounds and comparable graphemes (i.e., visual letters) of the same phonetic label. Given that linguistic experience shapes categorical processing, and letter-speech sound matching plays a crucial role during early reading acquisition, we hypothesized sound phoneme and visual grapheme tokens representing the same linguistic identity might recruit common neural substrates, despite originating from different sensory modalities. Behavioral and neuroelectric brain responses (ERPs) were acquired as participants categorized stimuli from sound (phoneme) and homologous letter (grapheme) continua each spanning a /da/-/ga/ gradient. ⋯ Auditory and visual categorization also recruited common visual association areas in extrastriate cortex but in opposite hemispheres (auditory = left; visual = right). Our findings reveal both auditory and visual sensory cortex supports categorical organization for phonetic labels within their respective modalities. However, a partial overlap in phoneme and grapheme processing among occipital brain areas implies the presence of an isomorphic, domain-general mapping for phonetic categories in dorsal visual system.