Androgen cell signaling pathways involved in neuroprotective actions

Christian J. Pike, Thuy Vi V. Nguyen, Martin Ramsden, Mingzhong Yao, M. Paul Murphy, Emily R. Rosario

Research output: Contribution to journalReview articlepeer-review

106 Scopus citations


As a normal consequence of aging in men, testosterone levels significantly decline in both serum and brain. Age-related testosterone depletion results in increased risk of dysfunction and disease in androgen-responsive tissues, including brain. Recent evidence indicates that one deleterious effect of age-related testosterone loss in men is increased risk for Alzheimer's disease (AD). We discuss recent findings from our laboratory and others that identify androgen actions implicated in protecting the brain against neurodegenerative diseases and begin to define androgen cell signaling pathways that underlie these protective effects. Specifically, we focus on the roles of androgens as (1) endogenous negative regulators of β-amyloid accumulation, a key event in AD pathogenesis, and (2) neuroprotective factors that utilize rapid non-genomic signaling to inhibit neuronal apoptosis. Continued elucidation of cell signaling pathways that contribute to protective actions of androgens should facilitate the development of targeted therapeutic strategies to combat AD and other age-related neurodegenerative diseases.

Original languageEnglish
Pages (from-to)693-705
Number of pages13
JournalHormones and Behavior
Issue number5
StatePublished - May 2008

Bibliographical note

Funding Information:
This work was supported by NIA grant AG23739 (CJP). ERR was supported by NS52143.


  • Alzheimer's disease
  • Androgen
  • Cell signaling
  • Neuroprotection
  • Testosterone
  • β-amyloid

ASJC Scopus subject areas

  • Endocrinology
  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience


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