Figure 2.

Combined theory in the neurodegenerative diseases.

Misfolded protein aggregates can bind and activate a whole range of PRRs triggering neuroinflammation. In the brain parenchyma, when the innate immunity microglia-mediated and adaptive immunity, regulated by the BBB, the CP and the Treg functionality, are not decisive, the toxic cascade and neuronal death have been demonstrated. Therefore, a relationship among amyloid-like deposition, immune mechanisms and neurodegenerative pathologies has been described. Source: Servier Medical Art by Servier and modified under the following terms: Creative Commons Attribution 3.0 Unported license (CC BY 3.0). AD: Alzheimer’s disease; Aβ: amyloid β protein; α-syn: α-synuclein; ALS: amyotrophic lateral sclerosis; BBB: blood-brain barrier; CP: choroid plexus; FTLD: Frontotemporal lobar degeneration; FUS: fused in sarcoma gene; LBD: Lewy body disease; MSA: multiple system atrophy; PD: Parkinson’s disease; PRRs: Pattern-recognition receptors; SOD1: superoxide dismutase 1; TDP-43: transactive response DNA binding protein with a molecular weight of 43 kDa; Teff: effector T cell; TLR: toll-like receptor; Treg: regulatory T cell.