ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1989.tb04873.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Clinical investigation of late onset Alzheimer's disease requires establishment of simple clinical and laboratory diagnostic criteria as neuropathological confirmation is not possible in the ordinary victim. Explicit criteria for the selection of mildly impaired victims in a 4‐month trial of treatment and the need for new, more careful methods of dementia typing are discusse

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1989.tb04874.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

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 ne

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1989.tb04875.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Sixteen patients diagnosed clinically and in the laboratory as having Alzheimer's disease (AD) of late onset (>70 years of age) type, were given drugs twice a day for sixteen weeks, in a double blind design. Seven patients were given lecithin (62% phosphatidyl choline) and choline chloride and 4 patients placebo. Five patients were first treated with lecithin and choline chloride for four weeks, then L‐dopa combined with benserazide hydrochloride was added for four weeks and finally L‐tryptophan was also given for eight weeks (per day mean ± SEM: 26 ± 0.53 g, 53 ± 1.7 mmol, 0.71 ± 0.050 mmol, 4.1 ± 0.30 mmol). In addition, nicotinamide, sodium salicylate and benserazide hydrochloride were given (per day: 8.2 mmol, 9.4 mmol and mean ± SEM: 40 ± 2.8 mg, respectively). Side reactions were studied twice a week, behavior and chemical effects from blodd and urine samples and after 8 and 16 weeks of treatment. The three precursors, which were intended to increase cholinergic, dopaminergic and serotonergic activities in brain. Two of these precursors, lecithin and phosphatidyl choline, are found in ordinary food and the third, L‐dopa, is normally produced by in vivo oxidation of L‐tyrosine in food. Lecithin and choline chloride did not decrease food intake, but these substances combined with L‐tryptophan did so, as did L‐dopa. The lecithin and choline chloride treatment increased the fasting plasma levels of choline and low density lipoprotein cholesterol but did not change the urinary excretions of cortisol, homovanillic acid (HVA), 5‐hydroxyindoleacetic acid (5‐HIAA), norepinephrine and epineph‐rine. The addition of L‐dopa and L‐tryptophan increased the urinary excretions of HVA, and 5‐HIAA and probably also the norepinephrine excretion. This complete multisubstitution schedule decreased the urinary excretion of epinephrine, did not change cortisol excretion and seemed to increase the urinary excretion ratios of HVA to 3‐methoxy‐4‐hydroxy‐mandelic acid (HMMA) and to HMMA + 3‐methoxy‐4‐hydroxyphenylglycol (MHPG). These increases were, however, not significant There were no consistent effects on the cognitive functions or performance with thi

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1989.tb04876.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

In patients with early stages of Alzheimer's disease (AD), late onset type, ordinary blood analyses such as hemoglobin, blood cell sedimentation rate, level of HbA1c, leucocyte and platelet concentrations and serum levels of sodium, potassium, calcium, phosphate, creatinine, haptoglobin, aspartate amino transferase, lactate dehydrogenase, cobal‐amines, folic acid, free thyroxine, and thyroid stimulating hormone showed similar average levels as in age matched, healthy controls. Erythrocyte mean corpuscular volume was lower in the late onset AD patients but was still within normal range (for middle‐aged persons). Serum albumin was in the normal range (for middle‐aged persons) in the late onset AD patients but significantly higher when compared to the controls. Serum levels of glucose, total protein, bilirubin, alkaline phosphatase, iron, total iron binding capacity were in the normal range (for middle‐aged persons) in these AD patients. Serum levels of growth hormone and cortisol in late onset AD were significantly increased in the morning when compared to the afternoon levels. Serum estradiol was significantly reduced in male late onset AD patients when compared to controls. Cholinesterase activity in plasma and erythrocytes was significantly decreased, and the ratio of cholinesterase activity in plasma over that in erythrocytes was at the same average level as in the controls. Urinary excretions of cortisol and epinephrine were significantl

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1989.tb04877.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Psychometric profiles of 18 patients with Alzheimer's disease (AD). late onset type, and of 13 healthy control subjects were compared. Clear achievement reductions were found for the late onset AD patients in tests of face recognition and continuously measured reaction time (simple as well as choice). Also, the new time‐order error (TOE) test was utilized. From comparisons between computer‐presented successive stimuli, this test yields scores indicating basic perceptual/cognitive processes, as well as achievement scores. The TOE‐test results indicated a lowered capacity of attention and of perceptual adaptation in the late onset AD patients for tone duration, but not for line length. A comparison with a previous study of solvent‐related brain dysfunction suggests the potential value of TOE tests for differential diagnosis in d

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1989.tb04878.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1989.tb04879.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1989.tb04880.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY