The relationship between cognition and immunity is long-standing and extends from phenomenology to molecular mechanisms. Current concepts on this relationship indicate that immunoevasion mechanisms targeting innate immunity and proteostasis remain as lasting implications of infection, and either trigger or enhance neurodegenerative processes. The COVID-19 pandemic has further served to outline this relationship, with an unprecedented amount of data on how exposure to a viral pathogen may impact cognition and trigger molecular events and neuropathology closely resembling those of neurodegenerative disease. Furthermore, homeostatic type I interferon signaling in the CNS is a known and conserved target for various pathogens, with its dysregulation directly effecting cognitive and affective phenomena. Interestingly, recent developments in Alzheimer’s disease research have uncovered both novel and central roles for innate immune mechanisms such as interferon signaling in its pathogenesis – indicating that infection, cognition and neurodegeneration are deeply interconnected.

There is an urgent need to systematically synthesize these parallel fields of research in immunity and neurodegenerative disease. Epidemiological data, mainly driven by COVID-19 research reveal potentially lasting effects of pathogen exposure on cognition, with candidate mechanisms involving immune dysregulation rather than lasting infection. Furthermore, neuropathological and molecular studies corroborate on the overlap between neurodegenerative disease and COVID-19. Current evidence on these mechanisms suggests a convergence on immunity, presenting a unique opportunity to understand how infection can affect cognition, and trigger neurodegeneration. As pathogen exposure appears to be an early step of the process, we may stand to gain a novel class of therapeutics by their study.

In this Research Topic, we aim to explore both epidemiological data and mechanisms that explore the relationship between cognition, neurodegeneration, and infection. Authors should focus on specific aspects, such as:

1. Observational studies on the relationship between cognition and infection exposure, including but not limited to COVID-19.
2. Basic science or translational studies on specific mechanisms that link cognitive impairment, neurodegeneration and immune mechanisms, with a specific interest in type I interferon signaling and innate immunity.
3. Computational biology studies of shared mechanisms between neurodegenerative infectious disease, with a specific interest in dementias.

Types of Manuscripts: 1) Review articles and 2) Original manuscripts

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Frontiers in Human Neuroscience

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