Ginkgo biloba leaf extract (EGb 761) has demonstrated neuroprotective effects in a Ginkgo biloba 525

variety of studies ranging from molecular and cellular, to animal and human; © 2007 Elsevier Australia

however, the cellular and molecular mechanisms remain unclear (Smith et al 2002). Of the constituents studied, it appears that the bilobalide constituent is chiefly responsible for this activity, although others are also involved (DeFeudis & Drieu 2000).

Up until recently, it was believed that the antioxidant, membrane stabilising and platelet-activating factor antagonist effects were chiefly responsible for neuroprotection, but new evidence suggests MAO inhibitor activity and effects at the mitochondria may also be important contributing mechanisms. Beta-amyloid Ginkgo biloba extract EGb 761 protects cells against toxicity induced by beta-amyloid in a concentration-dependent manner, according to in vitro tests (Bastianetto & Quirion 2002a, b, Bastianetto et al 2000). More recently in vivo studies have confirmed that ginkgo extract has an anti-amyloid aggregation effect (Luo 2006). It appears that ginkgo increases transthyretin RNA levels in mouse hippocampus, which is noteworthy because transthyretin is involved in the transport of beta-amyloid and may provide a mechanism to reduce amyloid deposition in brain (Watanabe et al 2001). There is also evidence that G. biloba modulates alpha-secretase, the enzyme that cuts the amyloid precursor protein and prevents amyloidogenic fragments from being produced (Colciaghi et al 2004). Cerebral ischaemia There is evidence from experimental and clinical studies that G. biloba extract protects tissues from ischaemia/reperfusion damage (Janssens et al 2000). According to investigation with an experimental model, EGb 761 could prevent and treat acute cerebral ischaemia, but the effect was most pronounced when administered prophylactically (Peng et al 2003).

Stabilisation and protection of mitochondrial function Several in vitro tests have demonstrated that EGb 761 stabilises and protects mitochondrial function (Eckert et al 2005, Janssens et al 2000). These observations are gaining the attention of researchers interested in neurodegenerative diseases as it is suspected that the mitochondria and the phenomenon of mitochondrial permeability transition play a key role in neuronal cell death and the development such diseases (Beal 2003, Shevtsova etal 2005).

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