Stem cell-derived extracellular vesicles (EVs) are capable of exerting therapeutic effects in amyotrophic lateral sclerosis. EVs can modulate oxidative stress mechanisms, mitochondrial apoptotic pathways, and inflammatory signaling processes.

Weeks or months after acute infection with severe acute respiratory syndrome coronavirus 2, the patient presented increased levels of pro-inflammatory cytokines and neutrophils in the cerebrospinal fluid and blood, with jugular vein thrombosis as a possible sequela of long coronavirus disease 2019.

The Alzheimer's Disease Neuroprotection Research Initiative's objective is to facilitate coordinated, multidisciplinary efforts to develop systemic neuroprotective strategies to combat AD. The aim is to achieve mitigation of the full spectrum of pathological processes underlying AD, with the goal of halting or even reversing cognitive decline. The main neuroprotective intervention targets for AD including NTFs, antineuroinflammation, astrocytic protection, remyelination, stem-cell therapy and in vivo neural regeneration, cerebral glucose metabolism regulation, vascular system protection, lymphatic protection, prion-like proteinopathy regulation, peripheral neurotoxic substances clearance, systemic NTFs, and physical exercise, as well as food and nutrition. Investigations into advanced neuroimaging techniques for earlier and more precise characterization of molecular events at scales ranging from cellular to the full system level are equally important as it is necessary for the evaluation of the beneficial effects of different neuroprotective intervention approaches. AD, Alzheimer's disease; CNTF, ciliary neurotrophic factor; DHA, docosahexaenoic acid; GDF11, growth differentiation factor 11; GDNF, glial cell-derived neurotrophic factor; IFN-γ, interferon-γ; NTFs, neurotrophic factors; ROS, reactive oxygen species; TNF-α, tumor necrosis factor-α.

Monocytes and monocyte-derived cells in hypoxic-ischemic encephalopathy (HIE) and neonatal arterial ischemic stroke (NAIS). (A) The origin of monocytes infiltrating the brain in neonatal HIE and NAIS has yet to be investigated, including the possibility that they originate from various sources, such as the spleen and bone marrow. (B) Monocytes can infiltrate the brain through different routes, but it is not yet known whether they can migrate from the meninges to the brain parenchyma after HIE and NAIS. (C) Monocytes infiltrate the brain in the first hours and days following HIE and NAIS, and chronic monocyte infiltration has been observed in HIE models. Monocytes can differentiate into macrophages and microglia-like cells, which can persist in the brain during the chronic phase of NAIS and HIE.