Lipocalin 2 regulates iron homeostasis, neuroinflammation, and insulin resistance in the brains of patients with dementia: Evidence from the current literature.
Daejin LimJae-Ho JeongJuhyun SongPublished in: CNS neuroscience & therapeutics (2021)
Dementia accompanied by memory loss is considered one of the most common neurodegenerative diseases worldwide, and its prevalence is gradually increasing. Known risk factors for dementia include genetic background, certain lifestyle and dietary patterns, smoking, iron overload, insulin resistance, and impaired glucose metabolism in the brain. Here, we review recent evidence on the regulatory role of lipocalin 2 (LCN2) in dementia from various perspectives. LCN2 is a neutrophil gelatinase-associated protein that influences diverse cellular processes, including the immune system, iron homeostasis, lipid metabolism, and inflammatory responses. Although its functions within the peripheral system are most widely recognized, recent findings have revealed links between LCN2 and central nervous system diseases, as well as novel roles for LCN2 in neurons and glia. Furthermore, LCN2 may modulate diverse pathological mechanisms involved in dementia. Taken together, LCN2 is a promising therapeutic target with which to address the neuropathology of dementia.
Keyphrases
- mild cognitive impairment
- cognitive impairment
- insulin resistance
- metabolic syndrome
- systematic review
- type diabetes
- traumatic brain injury
- spinal cord
- risk factors
- adipose tissue
- gene expression
- physical activity
- high fat diet
- skeletal muscle
- weight loss
- polycystic ovary syndrome
- dna methylation
- genome wide
- lipopolysaccharide induced
- lps induced
- high fat diet induced