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Early Stages of Late Onset Alzheimer's Disease

In order to study protein metabolism, plasma levels of 22 amino acids were measured with high pressure chromatography in old patients with Alzheimer's disease (AD) of late onset andin early stages of development. Derangements were observed in protein metabolism in 16 non‐treated patients when compared with 7 age matched healthy controls. There were increased fasting levels of plasma cystine and decreased fasting levels of plasma tyrosine and plasma tryptophan. The ratio of fasting levels of plasma tryptophan to the sum of plasma phenylalanine, tyrosine, leucine, isoleucine and valine was significantly decreased, and the ratio of fasting levels of plasma tyrosine to the sum of tryptophan, phenylalanine, leucine, isoleucine and valine was low but was not significantly decreased when compared to controls. Normal fasting levels were observed for plasma taurine, threonine, serine, aspargine+glutamate, glutamine, glycine, alanine, citrulline, alpha‐aminobutyrate, valine, metionine, isoleucine, leucine, phenylalanine, ornithine, lysine, 1‐M‐histidine, histidine, arginine and proline. Since tryptophan and tyrosine are precursors of dopamine/norepinephrine and serotonine, respectively, these monaminergic activities in the central nervous system (CNS) might be reduced in early stages of late onset AD. These observations made us think that there was need for a trial with precursor loading to reduce the tryptophan and tyrosine deficiencies, possibly, thereby increasing mental capacity and performance (see this study and study III). Urine excretion of 5‐hydroxyindoleacetic acid (5‐HIAA) was increased in untreated late onset AD patients. An increased tryptophan metabolism may thus be a part of the explanation for the reduced serum levels. The patients were given L‐tryptophan (4.1 ± 0.30 mmol per 24 h, mean ± SEM) for eight weeks in a double‐blind trial. As expected the tryptophan administration further increased urine excretion of 5‐HIAA. However, this treatment regimen did not increase fasting plasma level of tryptophan nor the ratio of tryptophan to the sum of phenylalanine, tyrosine, leucine, isoleucine, and valine. However, with the dose given the treatment did not significantly improve mental function, or performance. These observations in mild to early moderate stages of late onset AD are in agreement with previous reports. The derangement in cystine production as indicated by increased plasma levels of cystine is a new observation in AD.