TrAC Trends in Analytical Chemistry, Год журнала: 2024, Номер unknown, С. 118096 - 118096
Опубликована: Дек. 1, 2024
Язык: Английский
TrAC Trends in Analytical Chemistry, Год журнала: 2024, Номер unknown, С. 118096 - 118096
Опубликована: Дек. 1, 2024
Язык: Английский
Journal of Neuroimmune Pharmacology, Год журнала: 2025, Номер 20(1)
Опубликована: Фев. 4, 2025
Abstract Multiple sclerosis (MS) is a central nervous system (CNS) autoimmune disorder, with limited treatment options. This disease characterized by differential pathophysiology between grey matter (GM) and white (WM). The predominant WM hallmark the perivascular plaque, associated blood brain barrier (BBB) loss of function, lymphocytic infiltration, microglial reactivity, demyelination axonal injury adequately addressed immunomodulatory drugs. By contrast, mechanisms underlying GM damage remain obscure, consequences for neuroprotective strategies. Cortical pathology already significant in early MS reduced BBB disruption infiltration relative to WM, but highly inflammatory environment, neuro/axonal loss. There no satisfactory explanation occurrence neurodegeneration without large-scale cell influx cortical GM. A candidate mechanism suggests that it results from soluble factors originating meningeal aggregates, which diffuse into tissue trigger activation. However, recent literature highlights role platelets inflammation, together relationship coagulation factors, particularly fibrinogen, MS. Using experimental encephalomyelitis (EAE) model, we identified as drivers neuroinflammation platelet-neuron associations pre-symptomatic stage. We propose fibrinogen leakage across signal platelet represent major participant neurodegeneration. concept compatible new appreciation immune cells neuronal driven sequestered meninges. Graphical
Язык: Английский
Процитировано
1TrAC Trends in Analytical Chemistry, Год журнала: 2024, Номер unknown, С. 118096 - 118096
Опубликована: Дек. 1, 2024
Язык: Английский
Процитировано
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