Toward a nomenclature consensus for diverse intelligent systems: Call for collaboration.

Disagreements about language use are common both between and within fields. Where interests require multidisciplinary collaboration or the field of research has the potential to impact society at large, it becomes critical to minimize these disagreements where possible. The development of diverse intelligent systems, regardless of the substrate (e.g., silicon vs. biology), is a case where both conditions are met. Significant advancements have occurred in the development of technology progressing toward these diverse intelligence systems. Whether progress is silicon based, such as the use of large language models, or through synthetic biology methods, such as the development of organoids, a clear need for a community-based approach to seeking consensus on nomenclature is now vital. Here, we welcome collaboration from the wider scientific community, proposing a pathway forward to achieving this intention, highlighting key terms and fields of relevance, and suggesting potential consensus-making methods to be applied.

Thyroid hormone-dependent oligodendroglial cell lineage genomic and non-genomic signaling through integrin receptors.

Multiple sclerosis (MS) is a heterogeneous autoimmune disease whereby the pathological sequelae evolve from oligodendrocytes (OLs) within the central nervous system and are targeted by the immune system, which causes widespread white matter pathology and results in neuronal dysfunction and neurological impairment. The progression of this disease is facilitated by a failure in remyelination following chronic demyelination. One mediator of remyelination is thyroid hormone (TH), whose reliance on monocarboxylate transporter 8 (MCT8) was recently defined. MCT8 facilitates the entry of THs into oligodendrocyte progenitor cell (OPC) and pre-myelinating oligodendrocytes (pre-OLs). Patients with MS may exhibit downregulated MCT8 near inflammatory lesions, which emphasizes an inhibition of TH signaling and subsequent downstream targeted pathways such as phosphoinositide 3-kinase (PI3K)-Akt. However, the role of the closely related mammalian target of rapamycin (mTOR) in pre-OLs during neuroinflammation may also be central to the remyelination process and is governed by various growth promoting signals. Recent research indicates that this may be reliant on TH-dependent signaling through ß1-integrins. This review identifies genomic and non-genomic signaling that is regulated through mTOR in TH-responsive pre-OLs and mature OLs in mouse models of MS. This review critiques data that implicates non-genomic Akt and mTOR signaling in response to TH-dependent integrin receptor activation in pre-OLs. We have also examined whether this can drive remyelination in the context of neuroinflammation and associated sequelae. Importantly, we outline how novel therapeutic small molecules are being designed to target integrin receptors on oligodendroglial lineage cells and whether these are viable therapeutic options for future use in clinical trials for MS.