Modelling cognitive deficits in Parkinson's disease: Is CA2 a gateway for hippocampal synucleinopathy?

Cinar E., Yalcin-Cakmakli G., Saka E., Ulusoy A., Yuruker S., ELİBOL B., ...More

EXPERIMENTAL NEUROLOGY, vol.330, 2020 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 330
  • Publication Date: 2020
  • Doi Number: 10.1016/j.expneurol.2020.113357
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
  • Keywords: Alpha-synuclein, Adeno-associated viral vector, Parkinson's disease, CA2 subregion, Synaptic dysfunction, Cognitive deficits, HUMAN ALPHA-SYNUCLEIN, ALZHEIMERS-DISEASE, NONMOTOR FEATURES, ANIMAL-MODELS, MOUSE MODEL, AREA CA2, DEMENTIA, PATHOLOGY, MEMORY, NEURODEGENERATION
  • Hacettepe University Affiliated: Yes


Background: Cognitive dysfunction is one of the most disabling non-motor symptoms of Parkinson's disease (PD), though its pathological correlates still remain elusive. Hippocampal Lewy pathology has recently been correlated by compelling evidence from post-mortem and imaging studies. Animal models recapitulating cognitive impairment in PD are essential to better understand the underlying pathophysiology. To investigate the hippocampal involvement in cognitive dysfunction of PD, we generated an experimental model by inducing midbrain and hippocampal alpha-synuclein pathology simultaneously.