SUMMARY There is a defect in tetrahydrobiopterin metabolism in brains from subjects with senile dementia of Alzheimer type compared to age-matched controls. This defect results in lowered total biopterin concentrations in brain. Brains from subjects with senile dementia of Alzheimer type retain their ability to synthesis neopterin and have normal dihydropteridine reductase activity, indicating a specific loss of ability to convert dihydroneopterin triphosphate to tetrahydrobiopterin.The synthesis of dopamine and noradrenaline in the brain is dependent upon the activity of tyrosine hydroxylase, and this in tum is regulated by the concentration of the hydroxylase cofactor, 5,6, 7, Protein was measured by the biuret method. Each brain sample was assayed for dihydropteridine reductase, BH4 synthesis activity, total neopterin and total biopterin.

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Chronic exposure to aluminium (Al) remains a controversial possible cause of sporadic forms of Alzheimer''s disease (AD). This article reviews the evidence that once Al enters the brain and individual brain cells, it may be involved in three pathological processes: (1) the production of abnormal forms of tau leading to the formation of cellular neurofibrillary tangles and neuropil threads; (2) the processing of the amyloid precursor protein, resulting in the formation of β-amyloid deposits and senile plaques, and (3) that via the mutual histocompatibility system, Al could be involved in the initiation of the immune response observed in AD patients. Despite recent evidence that Al could be involved in these processes, a conclusive case that exposure to Al initiates the primary pathological process in sporadic AD remains to be established.

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