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., ...Daha Fazla

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

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 330
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1016/j.expneurol.2020.113357
  • Dergi Adı: EXPERIMENTAL NEUROLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
  • Anahtar Kelimeler: 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 Üniversitesi Adresli: Evet

Özet

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.