Update on autoimmune dementia and its precursors

Abstract

Autoimmune dementia is a new disease entity increasingly coming into focus, and novel neural antibodies associated with dementia and its precursors have been described. However, the significance of these novel and emerging autoantibodies in conjunction with cognitive disorders is unclear. Antibodies such as Leucin-Rich, Glioma Inactivated 1 (LGI1) and N-Methyl-D-Aspartate Receptor (NMDAR) are already known to be pathogenic by triggering anomalies in synaptic plasticity and learning processes in animal models after having been transferred from humans to animals. In this review we describe various pathogenic mechanisms of antibodies such as complement dependent cytotoxicity, the internalization of membrane receptors, antagonistic effects, and alterations in vesicle endocytosis at the synaptic level. We also discuss established autoantibodies such as membrane-surface and intracellular antibodies in connection with cognitive disorders, as well as autoantibodies associated with neurodegenerative dementia, and autoimmune encephalitis with primary dementia syndrome. Test methods and the response to immunotherapy are also briefly explained. This overview provides a differentiated presentation of a heterogeneous dementia entity with its precursors, which requires more research to develop a differentiated treatment guideline.