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BACE1 Deficiency Causes Abnormal Neuronal Clustering in the Dentate Gyrus.

Stem cell reports | Jul 11, 2017

BACE1 is validated as Alzheimer's β-secretase and a therapeutic target for Alzheimer's disease. In examining BACE1-null mice, we discovered that BACE1 deficiency develops abnormal clusters of immature neurons, forming doublecortin-positive neuroblasts, in the developing dentate gyrus, mainly in the subpial zone (SPZ). Such clusters were rarely observed in wild-type SPZ and not reported in other mouse models. To understand their origins and fates, we examined how neuroblasts in BACE1-null SPZ mature and migrate during early postnatal development. We show that such neuroblasts are destined to form Prox1-positive granule cells in the dentate granule cell layer, and mainly mature to form excitatory neurons, but not inhibitory neurons. Mechanistically, higher levels of reelin potentially contribute to abnormal neurogenesis and timely migration in BACE1-null SPZ. Altogether, we demonstrate that BACE1 is a critical regulator in forming the dentate granule cell layer through timely maturation and migration of SPZ neuroblasts.

Pubmed ID: 28669600 RIS Download

Mesh terms: Amyloid Precursor Protein Secretases | Animals | Aspartic Acid Endopeptidases | Cell Adhesion Molecules, Neuronal | Cell Movement | Dentate Gyrus | Extracellular Matrix Proteins | Gene Deletion | Mice | Mice, Inbred C57BL | Nerve Tissue Proteins | Neural Stem Cells | Neurogenesis | Neurons | Serine Endopeptidases

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