A5039421466- Neuroscience and Neuropharmacology Research
- Alzheimer's disease research and treatments
- Cellular transport and secretion
- Vestibular and auditory disorders
- Prion Diseases and Protein Misfolding
- Protein Tyrosine Phosphatases
- Neuroendocrine regulation and behavior
- Chemokine receptors and signaling
- Memory and Neural Mechanisms
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Neuroscience of respiration and sleep
Seoul National University
2019-2023
Multiple brain regions are engaged in classical fear conditioning. Despite evidence for cerebellar involvement conditioning, the mechanisms by which outputs modulate learning and memory remain unclear. We identify a population of deep nucleus (DCN) neurons with monosynaptic glutamatergic projections to lateral parabrachial (lPBN) (DCN→lPBN neurons) mice. While optogenetic suppression DCN→lPBN impairs auditory memory, activation elicits freezing behavior only after Moreover, conditioning...
<title>Abstract</title> The cerebellum has recently been recognized for its role in non-motor functions, including classical fear conditioning. However, the molecular mechanisms underlying learning and memory remain largely unknown. Here, we investigate transcriptional changes associated with auditory Spatial transcriptomic analysis revealed that deep cerebellar nuclei (DCN), an output region of cerebellum, expression immediate early genes increased following retrieval, suggesting DCN may...
Abstract In tauopathy conditions, such as Alzheimer's disease (AD), highly soluble and natively unfolded tau polymerizes into an insoluble filament; however, the mechanistic details of this process remain unclear. brains AD patients, only a minor segment forms β‐helix‐stacked protofilaments, while its flanking regions form disordered fuzzy coats. Here, it is demonstrated that nucleation core (tau‐AC) sufficiently induced self‐aggregation recruited full‐length to filaments. Unexpectedly,...
In tauopathic conditions, such as Alzheimer's disease (AD), highly soluble and natively unfolded tau polymerizes into an insoluble filament; however, the mechanistic details of this process are not clear. AD brains, only a small segment forms -helix-stacked protofilaments, while its flanking regions form disordered fuzzy coats. Here, we demonstrated that nucleation core (tau-AC) sufficiently induced self-aggregation recruited full-length to filaments. Unexpectedly, phospho-mimetic tau-AC (at...
In tauopathic conditions, such as Alzheimer's disease (AD), highly soluble and natively unfolded tau polymerizes into an insoluble filament; however, the mechanistic details of this process are not clear. AD brains, only a small segment forms -helix-stacked protofilaments, while its flanking regions form disordered fuzzy coats. Here, we demonstrated that nucleation core (tau-AC) sufficiently induced self-aggregation recruited full-length to filaments. Unexpectedly, phospho-mimetic tau-AC (at...