Causes and consequences of disturbances of cerebral glucose metabolism in sporadic XXXX : therapeutic implications.

@entity5 @entity3072 @entity74 @entity195 @entity4044 @entity12689 @entity855
@entity195 is not a @entity74 . Etiologically, two different types or even diseases exist: inheritance in 5% to 10% of all Alzheimer cases versus 90% to 95% AD cases whith @entity5 ( @entity5 ). Different susceptibility genes along with adult lifestyle risk-factors- in the case of @entity5 the risk factor aging- may be assumed to cause the @entity74 . There is evidence that a disturbance in the insulin signal transduction pathway may be a central and early pathophysiologic event in @entity5 . Both, hypercortisolemia and increased adrenergic activity, in both old age and @entity5 may render the function of the neuronal insulin receptor vulnerable resulting in a diminished production of @entity855 . The reduced availability of @entity855 may damage the function of the endoplasmic reticulum/Golgi apparatus/trans Golgi network generating misfolded and malfolded proteins retained in the cell. In @entity5 , amyloid precursor protein is found to accumulate intracellularly thus not representing the cause but a driving force in the pathogenesis of @entity5 . Additionally, both disturbed insulin signaling and reduced @entity855 forward the hyperphosphorylation of tau protein. Thus, abnormalities in oxidative brain metabolism lead to the formation of two main morphologic hallmarks of @entity5 : senile plaques and @entity3072 . Therefore, the therapeutic goal in @entity5 should be the improvement of the neuronal energy state. Findings from both basic and clinical studies showed that @entity4044 extract ( @entity12689 ) may be appropiate to approach that goal.
