Adiponectin: a potential target for obesity-associated Alzheimer's disease.
Nikita Patil SamantGirdhari Lal GuptaPublished in: Metabolic brain disease (2021)
Obesity and dementia are two growing problems worldwide. Obesity act as a crucial risk factor for various diseases including Alzheimer's disease (AD). Several preclinical studies showed that middle-age obesity can be act as a possible feature of mild cognitive impairment in later years. Some studies have also demonstrated that a high-fat diet causes AD pathology, including extracellular amyloid-beta accumulation, hyperphosphorylation of tau, and cognition impairment. The correlation and molecular mechanism related to obesity-associated AD needs to be better evaluated. Presently, obesity results in an altered expression of several hormones, growth factors, and adipokines. Multiple signaling pathways such as leptin, insulin, adiponectin, and glutamate are involved to regulate vital functions in the brain and act as neuroprotective mediators for AD in a normal state. In obesity, altered adiponectin (APN) level and its associated downstream pathway could result in multiple signaling pathway disruption. Presently, Adiponectin and its inducers or agonist are considered as potential therapeutics for obesity-associated AD. This review mainly focuses on the pleiotropic effects of adiponectin and its potential to treat obesity-associated AD.
Keyphrases
- insulin resistance
- metabolic syndrome
- high fat diet
- weight loss
- high fat diet induced
- type diabetes
- mild cognitive impairment
- signaling pathway
- weight gain
- adipose tissue
- skeletal muscle
- cognitive decline
- machine learning
- small molecule
- poor prognosis
- physical activity
- body mass index
- long non coding rna
- brain injury
- cell therapy
- multiple sclerosis
- resting state
- cell proliferation
- pi k akt
- drug induced
- climate change
- blood brain barrier
- white matter
- functional connectivity
- risk assessment