英属哥伦比亚大学（UBC）科学家发现了阿尔茨海默病破坏大脑的新解——太多血管。
阿尔茨海默病新解：太多的血管
不管存在于血管壁或大脑组织中，细胞的凋亡已成为阿尔茨海默病的研究重点。Wilfred Jefferies小组揭示了神经退行性衰退可能是血管壁上细胞增殖所致。
观察阿尔茨海默病小鼠模型的脑组织，Jefferies 小组发现血管密度是正常小鼠的近2倍。与没患阿尔茨海默病的人类脑样本相比，死于此病的脑样本具有较高的血管密度。
论文发表在8月31日《PLoS One》期刊上，Jefferies 系统化地阐述了血管密布由β淀粉样蛋白刺激成的，这一蛋白已经成为阿尔茨海默病的标记分子。血-脑屏障的破裂是由血管生长或新血管生成引起的，而血-脑屏障允许携氧血液进入脑组织，同时阻止像病毒一样有害物质进入。
Jefferies 称，血管壁生长时，细胞就分裂增殖。在一分为二的分裂过程中，子细胞形状上暂时变成圆形，这就破坏血-脑屏障的完整性，有害物质就可能侵入脑组织中。
反过来说，破坏的屏障允许β淀粉样蛋白进入并沉淀，这些蛋白在脑神经元周围富集，最终杀死神经元。
之前的研究也谈到屏障的“渗漏”，但却把原因归结在血管壁上细胞凋亡，而不是细胞生长。（生物探索译 Pobee）
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生物探索推荐论文摘要
Evidence of reduced blood-brain barrier (BBB) integrity preceding other Alzheimer's disease (AD) pathology provides a strong link between cerebrovascular angiopathy and AD. However, the “Vascular hypothesis”, holds that BBB leakiness in AD is likely due to hypoxia and neuroinflammation leading to vascular deterioration and apoptosis. We propose an alternative hypothesis: amyloidogenesis promotes extensive neoangiogenesis leading to increased vascular permeability and subsequent hypervascularization in AD. Cerebrovascular integrity was characterized in Tg2576 AD model mice that overexpress the human amyloid precursor protein (APP) containing the double missense mutations, APPsw, found in a Swedish family, that causes early-onset AD. The expression of tight junction (TJ) proteins, occludin and ZO-1, were examined in conjunction with markers of apoptosis and angiogenesis. In aged Tg2576 AD mice, a significant increase in the incidence of disrupted TJs, compared to age matched wild-type littermates and young mice of both genotypes, was directly linked to an increased microvascular density but not apoptosis, which strongly supports amyloidogenic triggered hypervascularity as the basis for BBB disruption. Hypervascularity in human patients was corroborated in a comparison of postmortem brain tissues from AD and controls. Our results demonstrate that amylodogenesis mediates BBB disruption and leakiness through promoting neoangiogenesis and hypervascularity, resulting in the redistribution of TJs that maintain the barrier and thus, provides a new paradigm for integrating vascular remodeling with the pathophysiology observed in AD. Thus the extensive angiogenesis identified in AD brain, exhibits parallels to the neovascularity evident in the pathophysiology of other diseases such as age-related macular degeneration.
