Dementia: A neuroendocrine perspective

A. Polleri, M. V. Gianelli, Giovanni Murialdo

Research output: Contribution to journalArticlepeer-review


The etiology of Alzheimer's disease (AD) has not been as yet completely defined. Genetic, environmental and neurophysiological aspects should all be taken into account. The disease has also neuroendocrine implications, some of which are discussed in this review. It is known that stress and glucocorticoids may affect neurone survival. On the contrary, some data indicate that DHEA and DHEAS exert a neuroprotective action. In AD, changes in hypothalamic-pituitary-adrenal axis function have been reported. Experimental and clinical evidence indicates that glucocorticoid hypersecretion and DHEAS levels decrement may add to hippocampal dysfunction in aging and in AD. Glucocorticoid and β-amyloid concur in the mechanism of neurone damage, as well as excitatory amino acids (EAA), Ca ++ and reactive oxygen species (ROS). The neuroprotective effects exerted by IGFs are also hindered in aging and even more in AD. Production and biological actions of IGFs are negatively influenced by cortisol hypersecretion and DHEAS decrease in patients with AD.

Original languageEnglish
Pages (from-to)73-83
Number of pages11
JournalJournal of Endocrinological Investigation
Issue number1
Publication statusPublished - 2002


  • Aging
  • Alzheimer's disease
  • Cortisol
  • Hippocampus
  • IGF-I
  • Neurodegenerative diseases
  • Neurosteroids
  • Sex hormones

ASJC Scopus subject areas

  • Endocrinology


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