Brain Glucose Hypometabolism and Brain Iron Accumulation as Therapeutic Targets for Alzheimer's Disease and Other CNS Disorders

被引:0
|
作者
Rao, Indira Y. [1 ]
Hanson, Leah R. [1 ,2 ]
Frey II, William H. [1 ,2 ]
机构
[1] HealthPartners Ctr Memory & Aging, St Paul, MN 55130 USA
[2] HealthPartners Inst, Bloomington, MN 55425 USA
关键词
brain glucose hypometabolism; brain iron accumulation; Alzheimer's disease; intranasal insulin; intranasal deferoxamine; intranasal treatment; neuroinflammation; brain cell energy; nose-to-brain delivery; SPINAL-CORD-INJURY; INTRANASAL INSULIN; RAT MODEL; NEUROPATHIC PAIN; AMYLOID-BETA; DEFEROXAMINE; MEMORY; METABOLISM; DEMENTIA; HEME;
D O I
10.3390/ph18020271
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Two common mechanisms contributing to multiple neurological disorders, including Alzheimer's disease, are brain glucose hypometabolism (BGHM) and brain iron accumulation (BIA). Currently, BGHM and BIA are both widely acknowledged as biomarkers that aid in diagnosing CNS disorders, distinguishing between disorders with similar symptoms, and tracking disease progression. Therapeutics targeting BGHM and BIA in Alzheimer's disease can be beneficial in treating neurocognitive symptoms. This review addresses the evidence for the therapeutic potential of targeting BGHM and BIA in multiple CNS disorders. Intranasal insulin, which is anti-inflammatory and increases brain cell energy, and intranasal deferoxamine, which reduces oxidative damage and inflammation, represent promising treatments targeting these mechanisms. Both BGHM and BIA are promising therapeutic targets for AD and other CNS disorders.
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页数:12
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