中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (10): 1717-1718.doi: 10.4103/1673-5374.257527

• 观点:退行性病与再生 • 上一篇    下一篇

帕金森病的病理生理学的一个不同观点:一种令人沮丧的神经化学假设?

  

  • 出版日期:2019-10-15 发布日期:2019-10-15

A different view on the pathophysiology of Parkinson’s disease: a descendent neurochemical hypothesis?

Burak Yulug 1,2 , Mehmet Ozansoy 2, 3, Seyda Cankaya 1   

  1. 1Department of Neurology, Alanya Alaaddin Keykubat University, Antalya/Alanya, Turkey;
    2 Istanbul Medipol University, Restorative and Regenerative Medicine Center, Istanbul, Turkey;
    3 Department of Physiology, International School of Medicine, Istanbul Medipol University, Istanbul, Turkey
  • Online:2019-10-15 Published:2019-10-15
  • Contact: Burak Yulug, PhD, burakyulug@gmail.com

摘要:

orcid: 0000-0002-9704-6173 (Burak Yulug)

Abstract:

It has been already shown that Parkinson’s disease (PD) is characterized by a prominent degeneration in substantia nigra (SN) neurons. Growing evidence suggests that there is a latent period of PD associated with slight non-motor findings such as olfactory dysfunction . However, the potential biomarker role of olfactory dysfunction in PD has been a topic of great interest in the last years. The classical hypothesis of Braak suggests that PD begins as a synucleinopathy in the lower brainstem or in the olfactory bulb (OB) that progresses rostrally to the SN and amygdala to cause parkinsonism at a later stage of the disease. However, Braak’s hypothesis should be cautiously interpreted since this scheme is not based on the distribution of neuronal cell loss, but on the distribution of the accumulation of abnormal α-synuclein aggregates which leaves unanswered how it relates to the progression of neurochemical changes.