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. 2018 Apr 17;154(2):204–219. doi: 10.1111/imm.12922

Table 4.

Immune therapies in neuroinflammatory disorders

Therapeutic intervention Proposed mode of action Disease References
Antibodies to abnormal protein aggregations e.g. a‐synuclein, PrP Clearance of aggregates AD, prion diseases, HD, ALS, stroke, PND 132, 133, 134, 135
Plasmapheresis (+tumour removal) Removal of pathogenic antibody Paraneoplastic disorders 136
Stem cell therapy Creating non‐pathogenic and reparative cell populations MS, SMA, ALS, TBI, AD, PD, prion diseases, stroke, HD 137, 138, 139, 140, 141, 142, 143, 144
Antibiotics e.g. minocycline Inhibition of inflammation and anti‐apoptotic activity AD, ischaemia, PD, HD, MS 145, 146
Cannabinoids Attenuates excitotoxic glutamatergic neurotransmission, modulation of microglia and astrocytes AD, PD, HD, ALS, epilepsy, MS, autism 133, 147, 148, 149
Non‐steroidal anti‐inflammatory Inhibition of COX‐1 and ‐2 AD 132
Diet and calorie restriction Antioxidant functions, inhibits COX‐2 and iNOS, reduction in free radicals and oxidative stress Epilepsy, ALS, AD, PD 150, 151, 152, 153
Anti‐lymphocyte therapy B‐cell depletion (CD20)
Plasma cells depletion (CD19)
Blocking T‐cell responses
Modulating T‐cell phenotypes
MS, stroke, depression 135, 137, 154
Innate immunity based therapy Macrophage apoptosis and macrophage suppression. inhibition NLRP inflammasome inhibiting/modulating microglia phenotypes. MS, depression, ischaemia, TBI 137, 141, 154
Targeting ionotropic and metabotropic receptors Agonist/antagonist antibodies or ligands e.g. NMDA, glutamate receptor antagonist AD, PD, HD, MS, SMA, ALS, prion disease, epilepsy, bipolar disorder, TBI, depression, schizophrenia 132, 133, 134, 137, 138, 141, 154, 155, 156, 157, 158
Antioxidants Reducing ROS, upregulating antioxidant genes. Targeting Nrf2 pathway (e.g. BG12). HSPs. MS, HD, ALS, stroke, TBI, schizophrenia, depression
Friedreich's ataxia
134, 135, 137, 141, 154, 158, 159
RAGE antagonists Reduction of formation or activation of innate immune responses by blocking/inhibiting advanced glycation end‐products (AGEs) AD 160
Complement inhibition Blocking complement mediated neuronal damage Stroke, TBI, epilepsy 161, 162, 163
Potassium and sodium channel targets Neuroprotection e.g. lamotrigine, fampridine acid‐sensing ion channel 1 (ASIC1) MS 137
Chemokine/cytokine modulation Promoting regenerative microenvironment e.g. IL‐4, CD28, amplification of Tregs.
CXCR3
AD, TBI, epilepsy, depression, schizophrenia, bipolar disorder 132, 141, 154, 157, 158, 164