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Glial cells, including microglia and astrocytes, facilitate the survival and health of all cells within the central
nervous system (CNS) by secreting a range of growth factors and contributing to tissue and synaptic remodeling. Microglia
and astrocytes can also secrete cytotoxins in response to specific stimuli, such as exogenous pathogen-associated molecular
patterns (PAMPs), or endogenous damage-associated molecular patterns (DAMPs). Excessive cytotoxic secretions can induce the death of neurons and contribute to the progression of neurodegenerative disorders, such as Alzheimer’s disease
(AD). The transition between various activation states of glia, which include beneficial and detrimental modes, is regulated
by endogenous molecules that include DAMPs, cytokines, neurotransmitters, and bioactive lipids, as well as a diverse group
of mediators sometimes collectively referred to as resolution-associated molecular patterns (RAMPs). RAMPs are released
by damaged or dying CNS cells into the extracellular space where they can signal in autocrine and paracrine fashions by interacting with glial cell receptors. While the complete range of their effects on glia has not been described yet, it is believed
that their overall function is to inhibit adverse CNS inflammatory responses, facilitate tissue remodeling and cellular debris
removal. This article summarizes the available evidence implicating the following RAMPs in CNS physiological processes
and neurodegenerative diseases: cardiolipin (CL), prothymosin α (ProTα), binding immunoglobulin protein (BiP), heat
shock protein (HSP) 10, HSP 27, and αB-crystallin. Studies on the molecular mechanisms engaged by RAMPs could identify novel glial targets for development of therapeutic agents that effectively slow down neuroinflammatory disorders including AD.