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Changes in the Synaptic Proteome in Tauopathy and Rescue of Tau-Induced Synapse Loss by C1q Antibodies

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Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy

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Alzheimer’s Patient Microglia Exhibit Enhanced Aging and Unique Transcriptional Activation

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Complement C1q-dependent excitatory and inhibitory synapse elimination by astrocytes and microglia in Alzheimer’s disease mouse models

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Trem2 restrains the enhancement of tau accumulation and neurodegeneration by β-amyloid pathology

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Trem2 Deletion Reduces Late-Stage Amyloid Plaque Accumulation, Elevates the Aβ42:Aβ40 Ratio, and Exacerbates Axonal Dystrophy and Dendritic Spine Loss in the PS2APP Alzheimer's Mouse Model

Meilandt, W. J., Ngu, H., Gogineni, A., Lalehzadeh, G., Lee, S.-H., Srinivasan, K., Imperio, J., Wu, T., Weber, M., Kruse, A. J., et al. (2020) · The Journal of Neuroscience

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Lack of Widespread BBB Disruption in Alzheimer’s Disease Models: Focus on Therapeutic Antibodies

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A rare mutation in UNC5C predisposes to late-onset Alzheimer's disease and increases neuronal cell death

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Multiple sclerosis risk gene Mertk is required for microglial activation and subsequent remyelination

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TNF-α from inflammatory dendritic cells (DCs) regulates lung IL-17A/IL-5 levels and neutrophilia versus eosinophilia during persistent fungal infection

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Antibody-Mediated Targeting of Tau In Vivo Does Not Require Effector Function and Microglial Engagement

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Mice deficient in NRROS show abnormal microglial development and neurological disorders

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Neutral or Detrimental Effects of TREM2 Agonist Antibodies in Preclinical Models of Alzheimer’s Disease and Multiple Sclerosis

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