Table 1 The role of inflammatory factors in neurodegenerative diseases
From: Physiological and pathological consequences of exosomes at the blood–brain-barrier interface
Neurodegenerative diseases | Neuronal cargo | Activity | Inflammatory factors | Ref |
|---|---|---|---|---|
Alzheimer's disease (AD) | neurofibrillary tangles (NFT) and amyloid-beta peptide (Aβ) | Aggregates of hyperphosphorylated tau lead to ROS production and inflammatory responses | IL-1, IL-6, TNF-α, and PGE2 | [73] |
Parkinson’s disease (PD) | alpha-synuclein (α-syn) leads to the loss of dopaminergic neurons | Control of neurotransmitter release, through effects on the SNARE complex | C-reactive protein (CRP), IL-6, and TNF-α | [74] |
Amyotrophic lateral sclerosis | p75ECD phosphorylated neurofilament heavy (pNfH) neurofilament light (NfL) | Involved in neuroprotective actions against Aβ toxicity | CRP, IL-6, IL-8, TNF-α, IL-1β, IL-17, IL-33, IL-10, Monocyte chemoattractant protein 1 (MCP-1), and IFNγ | [75] |
Huntington's disease | rab11 activity | Affects the recycling of transferrin receptor and neuronal glutamate/cysteine transporter EAAC1 | IL-1, IL-6, TNF-α, TGF-β | [76] |
Lewy body disease | alpha-synuclein | localizes specifically to the nerve terminal and inhibits neurotransmitter release when over-expressed | IL-1β, TNF-α, IL-6, and IL-10 | [77] |
Multiple sclerosis (MS) | neutrophil-to-lymphocyte ratio | oligodendrocyte damage and demyelination | IL-6, IFN-γ, TNF-α, and granulocyte–macrophage colony-stimulating factor (GM-CSF) | [78] |