Table 4.

Immunotherapeutic approaches in neurodegenerative disorders

Treatment	Disease	Efficacy, expectations	References
Aβ antibody and T cells	AD	Clearance of Aβ aggregates	96,98
PrPSc antibody	Prion diseases	Inhibition of PrPSc aggregates	99
Αlpha synuclein antibody Modulation of microglial activation	PD	Inhibition of Lewy Body formation	100
Combination therapy, Plasmapheresis, Removal of tumour.	Paraneoplastic neurological disorders	Removal of anti-neuronal antibodies	101
Antibiotics Minocyclin	Neurodegeneration	Inhibition of inflammation and anti-apoptoic activity	102
Immunotherapy, Copaxone, IFN-β, Natalizumab, Cladribine, Ritixumab, Alemtuzumab, FTY 720	MS	Inhibition of specific T-cell and/or B-cell responses Inhibition of immune-cell entry into the CNS	103
Non-steroidal anti-inflammatory	AD	Inhibition of COX1 and COX-2	104,105
RAGE antagonists	AD	Reduction of formation or activation of innate immune responses by inhibiting/blocking AGEs	106
Glutamate antagonists	PD	Blocking glutamate	107
Anti-oxidants	Neurodegeneration	Reduction of oxidative stress	108,109
Complement inhibition	Stroke, TBI	Blocking complement-mediated neuronal damage	110,111
Cannabinoids	Huntington’s disease, MS	Attenuates excitotoxic glutamatergic neurotransmission	112,113
Diet, Calorific restriction	AD, PD	Antioxidant functions, Inhibits COX-2 and iNOS (Curcumin) Reduction in free radicals and oxidative stress	114–116

Aβ, amyloid-beta; AD, Alzheimer’s disease; AGE, advanced glycation end-products; CNS, central nervous system; COX, cyclooxygenase; IFN-β, interferon-β; iNOS, inducible nitric oxide synthase; MS, multiple sclerosis; PD, Parkinson’s disease; RAGE, receptor for AGE; TBI, traumatic brain injury.