Abstract
St. Johns Wort (SJW) has been used medicinally for over 5,000 years. Relatively recently, one of its phloroglucinol derivatives, hyperforin, has emerged as a compound of interest. Hyperforin first gained attention as the constituent of SJW responsible for its antidepressant effects. Since then, several of its neurobiological effects have been described, including neurotransmitter re-uptake inhibition, the ability to increase intracellular sodium and calcium levels, canonical transient receptor potential 6 (TRPC6) activation, N-methyl-D-aspartic acid (NMDA) receptor antagonism as well as antioxidant and anti-inflammatory properties. Until recently, its pharmacological actions outside of depression had not been investigated. However, hyperforin has been shown to have cognitive enhancing and memory facilitating properties. Importantly, it has been shown to have neuroprotective effects against Alzheimers disease (AD) neuropathology, including the ability to disassemble amyloid-β (Aβ) aggregates in vitro, decrease astrogliosis and microglia activation, as well as improve spatial memory in vivo. This review will examine some of the early studies involving hyperforin and its effects in the central nervous system (CNS), with an emphasis on its potential use in AD therapy. With further investigation, hyperforin could emerge to be a likely therapeutical candidate in the treatment of this disease.
Keywords: St. John's Wort, TRPC6 channels, NMDA receptors, amyloid aggregates, Alzheimer's transgenic mice
Current Medicinal Chemistry
Title: Neurobiological Effects of Hyperforin and its Potential in Alzheimers Disease Therapy
Volume: 17 Issue: 5
Author(s): T. N. Griffith, L. Varela-Nallar, M. C. Dinamarca and N. C. Inestrosa
Affiliation:
Keywords: St. John's Wort, TRPC6 channels, NMDA receptors, amyloid aggregates, Alzheimer's transgenic mice
Abstract: St. Johns Wort (SJW) has been used medicinally for over 5,000 years. Relatively recently, one of its phloroglucinol derivatives, hyperforin, has emerged as a compound of interest. Hyperforin first gained attention as the constituent of SJW responsible for its antidepressant effects. Since then, several of its neurobiological effects have been described, including neurotransmitter re-uptake inhibition, the ability to increase intracellular sodium and calcium levels, canonical transient receptor potential 6 (TRPC6) activation, N-methyl-D-aspartic acid (NMDA) receptor antagonism as well as antioxidant and anti-inflammatory properties. Until recently, its pharmacological actions outside of depression had not been investigated. However, hyperforin has been shown to have cognitive enhancing and memory facilitating properties. Importantly, it has been shown to have neuroprotective effects against Alzheimers disease (AD) neuropathology, including the ability to disassemble amyloid-β (Aβ) aggregates in vitro, decrease astrogliosis and microglia activation, as well as improve spatial memory in vivo. This review will examine some of the early studies involving hyperforin and its effects in the central nervous system (CNS), with an emphasis on its potential use in AD therapy. With further investigation, hyperforin could emerge to be a likely therapeutical candidate in the treatment of this disease.
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Cite this article as:
Griffith N. T., Varela-Nallar L., Dinamarca C. M. and Inestrosa C. N., Neurobiological Effects of Hyperforin and its Potential in Alzheimers Disease Therapy, Current Medicinal Chemistry 2010; 17 (5) . https://dx.doi.org/10.2174/092986710790226156
DOI https://dx.doi.org/10.2174/092986710790226156 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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