Sigma Ligands As Potent Inhibitors of Aβ and AβOs in Neurons and Promising Therapeutic Agents of Alzheimer’s Disease

The authors review the pathophysiology of Alzheimer’s disease and highlight the sigma ligands that display the capability of preventing or even reversing amyloid-β (Aβ) – and amyloid-β oligomers (AβOs) -induced neurotoxicity and blocking the signal transduction caused by AβOs.
[Neuropharmacology]
Ma, W.-H., Chen, A.-F., Xie, X.-Y., & Huang, Y.-S. (2020). Sigma ligands as potent inhibitors of Aβ and AβOs in neurons and promising therapeutic agents of Alzheimer’s disease. Neuropharmacology, 108342. https://doi.org/10.1016/j.neuropharm.2020.108342 Cite
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Neurotrope Announces First Patient Dosed in Long-Term Clinical Trial of Bryostatin in Alzheimer’s Disease

Neurotrope, Inc.announced dosing of the first patient in its ongoing, long-term Phase II study of Bryostatin-1 for the treatment of Alzheimer’s disease. The study was conducted in collaboration with the National Institutes of Health under a $2.7 million grant to Neurotrope.
[Neurotrope, Inc. (PR Newswire LLC)]
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The Effects of Microglia‐ and Astrocyte‐Derived Factors on Neurogenesis in Health and Disease

The authors describe how glial cells play a role in adult hippocampal neurogenesis in both health and disease, especially focusing on glia‐derived factors.
[European Journal of Neuroscience]
Araki, T., Ikegaya, Y., & Koyama, R. (2020). The effects of microglia‐ and astrocyte‐derived factors on neurogenesis in health and disease. European Journal of Neuroscience. https://doi.org/10.1111/ejn.14969 Cite
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Attenuation of the Extracellular Matrix Restores Microglial Activity during the Early Stage of Amyloidosis

Two‐photon vital microscopy demonstrated normal morphology and resting motility of microglia but strongly diminished number of microglial cells that migrated to the photolesion site in 5xFAD mice.
[Glia]
Stoyanov, S., Sun, W., Düsedau, H. P., Cangalaya, C., Choi, I., Mirzapourdelavar, H., Baidoe‐Ansah, D., Kaushik, R., Neumann, J., Dunay, I. R., & Dityatev, A. (n.d.). Attenuation of the extracellular matrix restores microglial activity during the early stage of amyloidosis. Glia, n/a(n/a). https://doi.org/10.1002/glia.23894 Cite
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UCB Enters into Collaboration with Roche to Develop Antibody Treatment for People Living with Alzheimer’s Disease

UCB today announced an agreement to enter into a world-wide, exclusive license agreement with Roche and Genentech, a member of the Roche Group, for the global development and commercialization of UCB0107 in Alzheimer’s Disease.
[UCB]
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AC Immune Advances phospho-Tau Alzheimer’s Vaccine in Phase Ib/IIa Study

AC Immune SA announced the initiation of the second highest dosing group in the company’s Phase Ib/IIa clinical trial evaluating ACI-35.030 for the treatment of Alzheimer’s disease.
[AC Immune]
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The Physiology, Pathology, and Potential Therapeutic Applications of the TREM2 Signaling Pathway

Investigators summarize and question what is known and remains to be discovered about the TREM2 signaling pathway, track the consequences of its activation in physiological niches and pathological contexts, and highlight the promising potential of therapeutic manipulation of TREM2 signaling.
[Cell]
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Reconstruction of the Human Blood-Brain Barrier In Vitro Reveals a Pathogenic Mechanism of APOE4 in Pericytes

Researchers revealed the role of pericytes in apolipoprotein (APOE4)-mediated cerebral amyloid angiopathy (CAA) and highlighted calcineurin-nuclear factor of activated T cells signaling as a therapeutic target in CAA and Alzheimer’s disease.
[Nature Medicine]
Blanchard, J. W., Bula, M., Davila-Velderrain, J., Akay, L. A., Zhu, L., Frank, A., Victor, M. B., Bonner, J. M., Mathys, H., Lin, Y.-T., Ko, T., Bennett, D. A., Cam, H. P., Kellis, M., & Tsai, L.-H. (2020). Reconstruction of the human blood–brain barrier in vitro reveals a pathogenic mechanism of APOE4 in pericytes. Nature Medicine, 1–12. https://doi.org/10.1038/s41591-020-0886-4 Cite
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Alzheimer’s-Associated PLCγ2 Is a Signaling Node Required for Both TREM2 Function and the Inflammatory Response in Human Microglia

The authors used genetically engineered human iPSC-derived microglia-like cells to show that triggering receptor expressed on myeloid cells 2 (TREM2) signaled through PLCγ2 to mediate cell survival, phagocytosis, processing of neuronal debris, and lipid metabolism.
[Nature Neuroscience]
Andreone, B. J., Przybyla, L., Llapashtica, C., Rana, A., Davis, S. S., van Lengerich, B., Lin, K., Shi, J., Mei, Y., Astarita, G., Di Paolo, G., Sandmann, T., Monroe, K. M., & Lewcock, J. W. (2020). Alzheimer’s-associated PLCγ2 is a signaling node required for both TREM2 function and the inflammatory response in human microglia. Nature Neuroscience, 1–12. https://doi.org/10.1038/s41593-020-0650-6 Cite
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Depletion of the AD Risk Gene SORL1 Selectively Impairs Neuronal Endosomal Traffic Independent of Amyloidogenic APP Processing

The authors validated defects in neuronal endosomal traffic by showing altered localization of amyloid precursor protein (APP) in early endosomes, a site of APP cleavage by the β-secretase.
[Cell Reports]
Depletion of the AD Risk Gene SORL1 Selectively Impairs Neuronal Endosomal Traffic Independent of Amyloidogenic APP Processing: Cell Reports. (n.d.). Retrieved June 4, 2020, from https://www.cell.com/cell-reports/fulltext/S2211-1247(20)30696-3 Cite
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Depletion of the AD Risk Gene SORL1 Selectively Impairs Neuronal Endosomal Traffic Independent of Amyloidogenic APP Processing

The authors validated defects in neuronal endosomal traffic by showing altered localization of amyloid precursor protein (APP) in early endosomes, a site of APP cleavage by the β-secretase.
[Cell Reports]
Depletion of the AD Risk Gene SORL1 Selectively Impairs Neuronal Endosomal Traffic Independent of Amyloidogenic APP Processing: Cell Reports. (n.d.). Retrieved June 4, 2020, from https://www.cell.com/cell-reports/fulltext/S2211-1247(20)30696-3 Cite
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