Journal
NEUROPSYCHOBIOLOGY
Volume 77, Issue 4, Pages 197-205Publisher
KARGER
DOI: 10.1159/000495521
Keywords
Alzheimer's disease; Hypothalamic-pituitary-adrenal axis; Hypothalamic-pituitary-gonadal axis; Insulin resistance; Glucose regulation
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Funding
- UPE-II, Ministry of Science and Technology (Government of India) [247]
- DST-PURSE-II, Ministry of Science and Technology (Government of India)
- DBT, Ministry of Science and Technology (Government of India) [BT/PR16164/NER/95/88/2015]
- SERB N-PDF Grant [PDF/2016/000670]
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Alzheimer's disease (AD), the commonest progressive neurodegenerative disorder of the brain, is clinically characterized by the formation of extracellular amyloid plaques and intracellular neurofibrillary tangles. Recent studies suggest a relationship between the endocrinal dysregulation and the neuronal loss during the AD pathology. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and hypothalamic-pituitary-gonadal (HPG) axis regulating circulating levels of glucocorticoid hormones has been implicated in the pathophysiology of AD. Likewise, dysregulated insulin signaling, impaired glucose uptake and insulin resistance are some of the prime factors in the onset/progression of AD. In this review, we have discussed the changes in HPA and HPG axes, implicated insulin resistance/signaling and glucose regulation during the onset/progression of AD. Therefore, simultaneous detection of these endocrinal markers in the early or presymptomatic stages may help in the early diagnosis of AD. This evidence for implicated endocrinal functions supports the fact that modulation of endocrinal pathways can be used as therapeutic targets for AD. Future studies need to determine how the induction or inhibition of endocrinal targets could be used for predictable neuroprotection in AD therapies. (C) 2019 S. Karger AG, Basel
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