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Locus Coeruleus (LC) is a brain nucleus that is involved in a variety of key functions (ranging from attention modulation to sleep-wake cycle regulation, to memory encoding); its proper function is necessary both during brain development and for brain integrity maintenance, and both at the microscale and macroscale level. Due to their specific intrinsic and extrinsic features, LC cells are considered particularly susceptible to damage concerning a variety of insults. This explains LC involvement in degenerative diseases not only in adults (in the context of neurodegenerative disease, mainly), but also in children (in relation to early hypoxic damage and Down's Syndrome, among others). In this narrative review, we dissect the potential mechanisms through which LC is affected in different diseases, with a special emphasis on the high rate of activity it is subjected to and the oxidative stress associated with it. Further research aimed at deepening our understanding of these mechanisms is needed to enable the development of potential strategies in the future that could slow down LC degeneration in subjects predisposed to specific brain disorders.
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http://dx.doi.org/10.3390/antiox14030255 | DOI Listing |
Sci Adv
September 2025
Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.
The locus coeruleus-norepinephrine (LC-NE) system regulates arousal and awakening; however, it remains unclear whether the LC does this in a global or circuit-specific manner. We hypothesized that sensory-evoked awakenings are predominantly regulated by specific LC-NE efferent pathways. Anatomical, physiological, and functional modularities of LC-NE pathways involving the mouse basal forebrain (BF) and pontine reticular nucleus (PRN) were tested.
View Article and Find Full Text PDFNeurotrauma Rep
August 2025
Department of Radiology, Weill Cornell Medicine; New York, New York, USA.
Traumatic brain injury (TBI) impairs attention and executive function, often through disrupted coordination between cognitive and autonomic systems. While electroencephalography (EEG) and pupillometry are widely used to assess neural and autonomic responses independently, little is known about how these systems interact in TBI. Understanding their coordination is essential to identify compensatory mechanisms that may support attention under conditions of neural inefficiency.
View Article and Find Full Text PDFPsychopharmacology (Berl)
September 2025
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad Universitaria, Mexico City, 04510, Mexico.
Rationale: One of the earliest changes associated with Alzheimer's disease (AD) is the loss of catecholaminergic terminals in the cortex and hippocampus originating from the Locus Coeruleus (LC). This decline leads to reduced catecholaminergic neurotransmitters in the hippocampus, affecting synaptic plasticity and spatial memory. However, it is unclear whether restoring catecholaminergic transmission in the terminals from the LC may alleviate the spatial memory deficits associated with AD.
View Article and Find Full Text PDFNeuropharmacology
September 2025
Department of Life Sciences, Ben-Gurion University of the Negev, 84105, Beer Sheva, Israel; Zelman Center for Brain Science Research, Ben-Gurion University of the Negev, 84105, Beer Sheva, Israel. Electronic address:
Norepinephrine (NE) is a key neuromodulator in the brain with a wide range of functions. It regulates arousal, attention, and the brain's response to stress, enhancing alertness and prioritizing relevant stimuli. In the auditory domain, NE modulates neural processing and plasticity in the auditory cortex by adjusting excitatory-inhibitory balance, tuning curves, and signal-to-noise ratio.
View Article and Find Full Text PDFJ Integr Neurosci
August 2025
Department of Neurobiology, Hebei Medical University, 050017 Shijiazhuang, Hebei, China.
Background: Sodium homeostasis is crucial for physiological balance, yet the neurobiological mechanisms underlying sodium appetite remain incompletely understood. The nucleus tractus solitarii (NTS) integrates visceral signals to regulate feeding behaviors, including sodium intake. This study investigated the role of 11β-hydroxysteroid dehydrogenase type 2 (HSD2)-expressing neurons in the NTS in mediating sodium appetite under low-sodium diet (LSD) conditions and elucidated the molecular pathways involved, particularly the cyclic adenosine monophosphate (cAMP)/mitogen-activated protein kinase (MAPK) signaling cascade.
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