期刊
NEUROLOGICAL SCIENCES
卷 34, 期 10, 页码 1719-1725出版社
SPRINGER-VERLAG ITALIA SRL
DOI: 10.1007/s10072-013-1454-1
关键词
Alzheimer's disease; Beta amyloid; Hyperphosphorylated tau; Insulin resistance; Long-term potentiation; Advanced glycation end products; Ferritin; JNK
Relentless progression of Alzheimer's disease (AD) poses a grave situation for the biomedical community to tackle. Agents starting as hot favorites in clinical trials have failed in later stages and it is time we reconsidered our approaches to intervene the disease. Quite some interesting work in the last decade has introduced a new school of thought which factors in neuronal glycemic imbalance as a major component for the development of AD. Insulin resistance in the brain has brought forward subsequent sequelae which might work towards amyloid accretion and/or tau hyperphosphorylation. It is also pointed out that insulin works by distributing iron to neuronal tissue and an insulin resistant state throws it off gear leading to iron overloading of neurons which is ultimately detrimental. A relatively recent investigation finds the role of c-Jun-N-terminal kinase (JNK3) in AD which also seems to bear a link with insulin resistance.
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