Sandra M. Cardoso

TL;DR: In this article , the role of bacterial-derived pathogen-associated molecular patterns (PAMPs) in Parkinson's disease etiology has been discussed, and it is shown that mesencephalic neurons exposed to an environmental alphaproteobacterium activate innate immunity through toll-like receptor 4 and Nodlike receptor 3.

TL;DR: A review of the latest advances on autophagy involvement in Parkinson's disease etiopathogenesis and potential disease-modifying strategies can be found in this paper, where the authors discuss potential disease modifying strategies.

TL;DR: Tacedinaline (Tac) as mentioned in this paper is a selective class I histone deacetylases (HDACs) inhibitor, which is shown to improve ER-Ca2+ retention and mitochondrial Ca2+ accumulation, mitochondrial depolarization and impaired ER-mitochondria cross-talk.

TL;DR: In this paper , a series of Rivastigmine-Benzimidazole (RIV-BIM) hybrids was reported as multitarget-directed ligands, thanks to their capacity to tackle important hallmarks of Alzheimer's disease.

Abstract: Neurons are postmitotic cells of long duration and therefore strongly dependent on intracellular quality control mechanisms, such as the autophagic pathway, to maintain their homeostasis. Autophagy, first described as a process primarily inducible by starvation, is an intracellular pathway that promotes the degradation of damaged organelles, pathogens, and protein aggregates. Much evidence associates mitochondrial and lysosomal dysfunction as well as protein misfolding in the etiopathogenesis of Parkinson's disease (PD), indicating that alterations in the autophagic pathway that promote the accumulation of toxic protein aggregates and dysfunctional organelles, such as mitochondria, may contribute to the PD neurodegenerative process. In this chapter we will review studies that clearly show that the autophagic pathway is compromised in PD as well as discuss which signaling autophagic pathways are altered and identify autophagic targets and modulators that may be used as future strategies for the disease.