Publications by authors named "Zhen-Xian Niou"

Article Synopsis
  • NMNAT2, a critical enzyme for NAD synthesis, is essential for the health of axons in glutamatergic neurons, which are often affected in neurodegenerative diseases.
  • Research showed that the loss of NMNAT2 leads to decreased ATP levels and impaired axonal transport, ultimately harming axonal integrity.
  • The study found that supplementing NAD or inhibiting the enzyme SARM1 can help restore axonal function and protect against degeneration caused by NMNAT2 deficiency.
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Background: Bioenergetic maladaptations and axonopathy are often found in the early stages of neurodegeneration. Nicotinamide adenine dinucleotide (NAD), an essential cofactor for energy metabolism, is mainly synthesized by Nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) in CNS neurons. NMNAT2 mRNA levels are reduced in the brains of Alzheimer's, Parkinson's, and Huntington's disease.

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Establishing a balance between excitation and inhibition is critical for brain functions. However, how inhibitory interneurons (INs) generated in the ventral telencephalon integrate with the excitatory neurons generated in the dorsal telencephalon remains elusive. Previous studies showed that INs migrating tangentially to enter the neocortex (NCx), remain in the migratory stream for days before invading the cortical plate during late corticogenesis.

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Allen Brain Atlas (ABA) provides a valuable resource of spatial/temporal gene expressions in mammalian brains. Despite rich information extracted from this database, current analyses suffer from several limitations. First, most studies are either gene-centric or region-centric, thus are inadequate to capture the superposition of multiple spatial-temporal patterns.

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