The roles of the immune system in brain maintenance and repair have become increasingly recognized over the last 20 years, especially within the context of Alzheimer’s disease (AD). Aging is the greatest risk factor for AD and is associated with the exhaustion/senescence of the adaptive immune system. Immune checkpoint activity can contribute to this exhaustion. The monoclonal antibody, IBC-Ab002, is directed against the PD-L1 immune checkpoint, the blockade of which evokes an interferon (IFN)-γ-dependent systemic immune response, which in turn recruits monocyte-derived macrophages to the brain. Preclinical data demonstrates that this immunological response can decrease levels of tau in tau transgenic animals and decrease levels of amyloid in amyloid transgenic animals, even in animals that lack TREM2 and therefore have inactive microglia. The results also showed reduced neuroinflammation, preservation of synapses, and improvements in cognitive performance that lasted around 4-6 weeks in mice. Jesse Cedarbaum, MD, FAAN, FANA, Yale University School of Medicine, New Haven, CT & Coeruleus Clinical Sciences LLC, Woodbridge, CT, explains the implications of this preclinical data in designing the first clinical trial (NCT05551741) testing IBC-Ab002 in 40 patients with early AD. This interview took place at the Clinical Trials on Alzheimer’s Disease congress 2022 in San Francisco.
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