Alpha-synuclein and iron: two keys unlocking Parkinson's disease.
Current therapies for Parkinson's disease (PD) confer symptomatic relief and are particularly efficient in the treatment of motor symptoms in earlier disease stages. However, we are still unable to treat the causes of neurodegeneration by modification of the underlying mechanisms, which is partially due to their insufficient understanding. In this short review, we focus on two pivotal disease mechanisms: alpha-synuclein pathology and dysfunction of iron homeostasis as well as their intricate interaction. Both pathomechanisms have been extensively studied in the past and represent valid targets for disease-modifying pharmacological treatment approaches for PD. We summarize the current attempts to exploit iron chelation and modification of alpha-synuclein pathology as translational therapies in PD and discuss the chances and challenges of prospective disease-modifying approaches.
Department of Neurology, University Medicine Göttingen, 37075, Göttingen, Germany. paul.lingor@med.uni-goettingen.de.|Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), Göttingen, Germany. paul.lingor@med.uni-goettingen.de.
Paul
0000-0001-9362-7096
P
Lingor
Department of Neurology, University Medicine Göttingen, 37075, Göttingen, Germany.|Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), Göttingen, Germany.
Eleonora
E
Carboni
Department of Neurology, University Medicine Göttingen, 37075, Göttingen, Germany.
Jan Christoph
JC
Koch
D000818:Animals; D000978:Antiparkinson Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D006801:Humans; D007501:Iron / Q000378:metabolism*; D010300:Parkinson Disease / Q000188:drug therapy* / Q000378:metabolism*; D051844:alpha-Synuclein / Q000378:metabolism*
D000978:Antiparkinson Agents; D051844:alpha-Synuclein; D007501:Iron
Disease mechanism; Neurodegeneration; Translational therapy