Researchers studying multiple sclerosis, Parkinson’s disease, and ischemic stroke are uncovering distinct biological processes that may be targeted to protect the nervous system. In newly diagnosed MS, protein changes in monocytes and B cells pointed to disrupted immune-cell communication early in the disease. In Parkinson’s disease, increasing proSAAS after motor symptoms had already developed slowed further decline and protected dopamine neurons in a rat model.
A third study focused on ischemic stroke, where GPR84 worsened blood-brain barrier damage, while blocking the receptor reduced leakage, swelling, and brain injury. Together, these findings highlight how immune signaling, protein protection, and vascular stability can each shape neurological damage and recovery. Identifying these disease-specific pathways may lead to more precise strategies for slowing progression and protecting vulnerable brain cells.
1. Cell-specific proteome profiling reveals altered peripheral immune cell communication in early multiple sclerosis
Researchers found distinct protein changes across major immune cells in newly diagnosed, untreated MS, with especially strong alterations in monocytes and B cells. The findings point to disrupted immune-cell communication as an early feature of MS and may reveal new targets for treatment development.
2. ProSAAS overexpression arrests progression of motor deficits in a rat alpha-synuclein model of Parkinson’s disease
Increasing proSAAS after motor symptoms had already developed stopped further motor decline and protected dopamine neurons in a rat model of Parkinson’s disease. The findings suggest this protein chaperone may help counter α-synuclein-related toxicity and warrants further study as a disease-modifying therapy.
3. GPR84 exacerbates blood-brain barrier disruption after ischemic stroke via cAMP/CREB-dependent tight junction suppression
Researchers found that GPR84 worsened blood-brain barrier damage after ischemic stroke, while removing or silencing the receptor reduced leakage, swelling, and brain injury. The findings identify GPR84 as a potential target for preserving the brain’s vascular barrier after stroke.
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