The Important Role of Lipids in Cognitive Impairment

The Important Role of Lipids in Cognitive Impairment

Jia Yu (Peking University, China & Beijing Geriatric Hospital, China), Zheng Chen (Beijing Geriatric Hospital, China), Jiangyang Lu (First Affiliated Hospital of General Hospital of PLA, China), Tingting Liu (Peking University, China), Liang Zhou (Peking University, China), Xinying Liu (Peking University, China), Miao Sun (Peking University, China), Weizhong Xiao (Third Hospital of Peking University, China), Dongsheng Fan (Third Hospital of Peking University, China) and Dehua Chui (Peking University, China & Third Hospital of Peking University, China)
Copyright: © 2013 |Pages: 5
DOI: 10.4018/978-1-4666-3604-0.ch014
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The current knowledge base on circulating serum and plasma risk factors of the cognitive decline of degenerative Alzheimer’s Disease is linked to cholesterol homeostasis and lipoprotein disturbances (i.e., total cholesterol, 24S-hydroxy-cholesterol, lipoprotein(a), or apolipoprotein E. Lipoprotein lipase (LPL) is also expressed in the brain, with the highest levels found in the pyramidal cells of the hippocampus, suggesting a possible role for LPL in the regulation of cognitive function. Little is currently known, however, about the specific role of LPL in the brain. The authors of this chapter have generated an LPL-deficient mouse model that was rescued from neonatal lethality by somatic gene transfer. The levels of the presynaptic marker synaptophysin were reduced in the hippocampus while the levels of the post-synaptic marker PSD-95 remained unchanged in the LPL-deficient mice. The decreased frequency of mEPSC in LPL-deficient neurons indicated that the number of presynaptic vesicles was decreased, which was consistent with the decreases observed in the numbers of total vesicles and docking vesicles. These findings indicate that LPL plays an important role in learning and memory function, possibly by influencing presynaptic function.
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The hippocampus-dependent learning and memory of LPL-deficient mice were studied by performance in the water maze and step-down passive avoidance tests. During the training sessions (days 1 and 2) for the water maze test, LPL-deficient mice spent a significantly longer amount of time than WT mice to find the terminal escape platform. There were no differences in the number of entries into the non-exit arms on day 1 of training between the two genotypes. The number of no-exit arm entries by the LPL-deficient mice significantly increased on day 2 of training. From days 3 to 7, both the latency to escape the platform and the frequency of entries into the no-exit arms by the LPL-deficient mice were significantly increased compared with those by the WT mice. There was a significant correlation between the latency to escape the platform and the number of errors. No changes in swim speed were observed during the training period. Taken together, these observations suggest that the increase in latency to platform is most likely due to the impairment of navigational strategy in the LPL-deficient mice. We further used a step-down inhibitory avoidance task to study the role of LPL in learning and memory. A significant decrease in the latency to step-down was observed in the LPL-deficient mice during the training trial. Similarly, a shortened retention time was observed in the LPL-deficient mice.

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