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Li Yang

Researcher at South China Normal University

Publications -  14
Citations -  1438

Li Yang is an academic researcher from South China Normal University. The author has contributed to research in topics: Amyloid precursor protein & Neurotransmission. The author has an hindex of 12, co-authored 14 publications receiving 1185 citations. Previous affiliations of Li Yang include Baylor College of Medicine.

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NFκB-Activated Astroglial Release of Complement C3 Compromises Neuronal Morphology and Function Associated with Alzheimer’s Disease

TL;DR: Dysregulation of neuron-glia interaction through NFκB/C3/C 3aR signaling may contribute to synaptic dysfunction in AD, and C3aR antagonists may be therapeutically beneficial.
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Selective clearance of aberrant tau proteins and rescue of neurotoxicity by transcription factor EB

TL;DR: It is demonstrated that TFEB effectively reduces neurofibrillary tangle pathology and rescues behavioral and synaptic deficits and neurodegeneration in the rTg4510 mouse model of tauopathy with no detectable adverse effects when expressed in wild‐type mice.
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Presynaptic and Postsynaptic Interaction of the Amyloid Precursor Protein Promotes Peripheral and Central Synaptogenesis

TL;DR: In vitro and in vivo studies identify APP as a novel synaptic adhesion molecule and postulate that transsynaptic APP interaction modulates its synaptic function and that perturbed APP synapticAdhesion activity may contribute to synaptic dysfunction and AD pathogenesis.
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Amyloid Precursor Protein Regulates Cav1.2 L-type Calcium Channel Levels and Function to Influence GABAergic Short-Term Plasticity

TL;DR: A critical role for APP is reported in the regulation of L-type calcium channels in GABAergic inhibitory neurons in striatum and hippocampus, and a direct link between APP and calcium signaling is provided and might help explain how altered APP regulation leads to changes in synaptic function that occur with AD.
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The Amyloid Precursor Protein Controls Adult Hippocampal Neurogenesis through GABAergic Interneurons

TL;DR: It is revealed that the APP plays an important role in the neural progenitor proliferation and newborn neuron maturation in the mouse dentate gyrus, and the findings indicate that APP dysfunction may contribute to impaired neurogenesis and cognitive decline associated with AD.