Linazasoro G
Centro de Investigación Parkinson, Fundación Dr. Carlos Elósegui, Policlínica Gipuzkoa, Parque Tecnológico Miramón, 174, 20009 San Sebastián, Gipuzkoa, Spain.
Parkinsonism Relat Disord. 2009 Jul;15(6):401-5. doi: 10.1016/j.parkreldis.2009.02.011. Epub 2009 Apr 5.
Neuroprotection in PD remains the most important goal of current research. Most of presently used strategies are directed at interfering with signalling pathways involved in neuronal death. However, the influence of compensatory alterations in neurotransmitter receptors and related signalling pathways, as well as the role of aging and associated lesions, are not taken into consideration. Their progressive failure might contribute to the appearance and/or progression of the disease. Thus, early restoration of basal ganglia physiology will support the compensatory events and delay the irreversible modification of circuitry that characterizes the clinical progression of PD. Enhancing neuronal plasticity and avoiding the negative effects of aging and associated lesions might help the remaining neural circuits to compensate for lost or broken circuits and improve overall network performance and neurological function. These modulating factors represent potential targets for therapeutic intervention resulting in lasting clinical benefit for the patient. The concept of neuroprotection should be modified, shifting the focus from neurons that are lost to those that survive.
帕金森病中的神经保护仍然是当前研究的最重要目标。目前使用的大多数策略都旨在干扰与神经元死亡相关的信号通路。然而，神经递质受体和相关信号通路的代偿性改变的影响，以及衰老和相关病变的作用，并未被考虑在内。它们的逐渐失效可能会导致疾病的出现和/或进展。因此，早期恢复基底神经节生理学将支持代偿性事件，并延迟表征帕金森病临床进展的神经回路的不可逆改变。增强神经元可塑性并避免衰老和相关病变的负面影响，可能有助于剩余的神经回路补偿丢失或受损的回路，并改善整体网络性能和神经功能。这些调节因素代表了治疗干预的潜在靶点，可为患者带来持久的临床益处。神经保护的概念应该被修正，将重点从死亡的神经元转移到存活的神经元上。
