The Neuroscience Laboratory, Felsenstein Medical Research Center, Sackler School of Medicine, Tel-Aviv University, Ramat Aviv, Israel.
Apoptosis. 2010 Nov;15(11):1415-21. doi: 10.1007/s10495-010-0491-y.
It has been well established that adult neurogenesis occurs throughout life in the subventricular (SVZ) and subgranular (SGZ) zones. However, the exact role of this type of brain plasticity is not yet clear. Many studies have shown that neurogenesis is involved in learning and memory. This has led to a hypothesis which suggests that impairment in memory during aging and neurodegenerative diseases such as Alzheimer's disease (AD) may involve abnormal neurogenesis. Indeed, during aging, there is an age-related decline in adult neurogenesis. This decline is mostly related to decreased proliferation, associated to decreased stimulation to proliferate in an aging brain. In AD, there is also evidence for decreased neurogenesis, that accompanies the neuronal loss characteristic of the disease. Interestingly in AD, there is increased proliferation, that may be caused by increasing amounts of soluble amyloid ß42-protein (Aβ₄₂). However, most of these new neurons die, and fibrillar Aβ₄₂ seems to be involved in generating an inappropriate environment for these neurons to mature. These findings open prospects for new strategies that can increase neurogenesis in normal or pathological processes in the aging brain, and by that decrease memory deficits.
成人神经发生发生在脑室下区(SVZ)和颗粒下区(SGZ)。然而,这种类型的脑可塑性的确切作用尚不清楚。许多研究表明,神经发生参与学习和记忆。这导致了一个假设,即衰老和神经退行性疾病(如阿尔茨海默病(AD))期间的记忆损伤可能涉及异常的神经发生。事实上,随着年龄的增长,成年神经发生会出现与年龄相关的下降。这种下降主要与增殖减少有关,与衰老大脑中增殖刺激减少有关。在 AD 中,也有证据表明神经发生减少,这伴随着该疾病的特征性神经元丧失。有趣的是,在 AD 中,增殖增加,这可能是由于可溶性淀粉样蛋白β₄₂-蛋白(Aβ₄₂)的含量增加引起的。然而,这些新神经元中的大多数都会死亡,纤维状 Aβ₄₂似乎参与生成不利于这些神经元成熟的不合适环境。这些发现为新策略提供了前景,这些策略可以增加衰老大脑中正常或病理过程中的神经发生,并由此减少记忆缺陷。