Brain Imaging In Human Aging, Alzheimer Disease And Rela

1. 利用正电子发射断层扫描（PET）的研究报道，人类的区域大脑葡萄糖代谢率（rCMRglc）随着健康衰老而下降。在这项研究中，我们发现这种下降可能反映了老年人的脑萎缩，因为在rCMRglc纠正萎缩后，它们不会发生。使用PET，我们测量了年轻和老年健康年轻男性在“休息”状态（蒙住眼睛，塞住耳朵）的rCMRglc之前和之后的萎缩校正。萎缩校正后无统计学意义的平均差异，但校正前无统计学意义。因此，与阿尔茨海默病不同，健康的人类衰老并不伴随着静息状态脑葡萄糖代谢的减少。

1. Studies with positron emission tomography (PET) have reported that regional cerebral metabolic rates for glucose (rCMRglc) decline with healthy aging in humans. In this study, we showed that such declines likely reflect brain atrophy in the elderly, as they do not occur after rCMRglc were corrected for atrophy. With PET, we measured rCMRglc, before and after correcting for atrophy, in young and older healthy young men while in the "resting" state (eyes covered and ears plugged). Statistically significant mean differences were absent after but not before atrophy correction. Thus, healthy human aging, unlike Alzheimer disease, is not accompanied by reduced resting-state brain glucose metabolism. 2. Brain synaptic activity and energy consumption decline in the course of Alzheimer disease. In a critical review, we proposed that in the first stage of disease, changes in synaptic function reduce neuronal energy demand and lead to potentially reversible downregulation of mitochondrial oxidative phosphorylation (OXPHOS). In a second stage, neurofibrillary tangles with abnormally phosphorylated tau protein accumulate within neuronal cytoplasm, until they co-opt the nonphosphorylated tau necessary for axonal transport of mitochondria between the cell nucleus and the synapse. Severe energy depletion leads to cell death.