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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For more than a century amyloid was considered to be an interesting, unique, but inconsequential pathologic entity that rarely caused significant clinical problems. We now recognize that amyloid is not one entity. In vivo it is a uniform organization of a disease, or process, specific protein co-deposited with a set of common structural components. Amyloid has been implicated in the pathogenesis of diseases affecting millions of patients. These range from Alzheimer's disease, adult-onset diabetes, consequences of prolonged renal dialysis, to the historically recognized systemic forms associated with inflammation and plasma cell disturbances. Strong evidence is emerging that even when deposited in local organ sites significant physiologic effects may ensue. With emphasis on A beta amyloid, we review the present definition, classification, and general in vivo pathogenetic events believed to be involved in the deposition of amyloids. This encompasses the need for an adequate amyloid precursor protein pool, whether precursor proteolysis is required prior to deposition, amyloidogenic amino acid sequences, fibrillogenic nucleating particles, and an in vivo microenvironment conducive to fibrillogenesis. The latter includes several components that seem to be part of all amyloids. The role these common components may play in amyloid accumulation, why amyloids tend to be associated with basement membranes, and how one may use these findings for anti-amyloid therapeutic strategies is also examined.
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PMID:A beta amyloidogenesis: unique, or variation on a systemic theme? 938 10

Amyloidoses are diseases, including some currently prominent such as Alzheimer's disease, bovine spongiform encephalophaty (BSE) and Type II diabetes, in which soluble proteins are deposited in a specific, highly stable, fibrillar form. The amyloid fibrils are made up of protofilaments whose molecular structure is composed of pairs of beta-sheets in a helical form that allows them to be continuously hydrogen-bonded along the length of the fibril. The observation that similar fibrils are generated from different proteins indicates that fibril formation is accompanied by structural conversion. The transmissible spongiform encephalopathies, such as BSE and kuru, involve an infectious agent identified with the prion protein. The properties of the agent are more consistent with prion amyloid than the protein itself, suggesting infectivity in these diseases in equivalent to the 'seeding' of amyloid fibrils at a new site.
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PMID:The molecular basis of amyloidosis. 944 39

Recent studies suggest that Alzheimer's disease and non-insulin-dependent (type 2) diabetes mellitus may share a common cell death mechanism, related to the toxicity of beta-amyloid (Abeta) and amylin, respectively. Both Abeta and amylin cause apoptosis in different cell culture systems, which may be related to the amyloidogenic properties of these peptides. We have further characterized the actions of a variety of Abeta peptides (Abeta25-35, Abeta1-40, Abeta1-42), human amylin and rat amylin (which does not form fibrils) on undifferentiated PC12 cells. Although all peptides except rat amylin compromised mitochondrial function as assessed by MTT reduction, only human amylin decreased cell viability at a concentration of 10 microM, as measured by lactate dehydrogenase release or trypan blue exclusion assay. The cell death caused by human amylin was determined to be predominantly of an apoptotic nature, with a possibility of a portion of necrotic cell death, which was not accompanied by increased expression of c-Jun or c-Fos inducible transcription factors.
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PMID:Acute application of human amylin, unlike beta-amyloid peptides, kills undifferentiated PC12 cells by apoptosis. 946 71

The benefits of hormone replacement therapy (HRT) in non-diabetic postmenopausal women are now well established. HRT improves climacteric symptoms and has beneficial effects on the cardiovascular system and the skeleton. In addition, recent studies suggest a reduced risk of Alzheimer's disease and colorectal cancer. Despite these beneficial effects, concerns continue regarding the increased risk of malignancy, thromboembolism and the possible deterioration in blood pressure. There are no long-term studies in women with diabetes who also receive HRT, so we cannot be certain of the benefits and risks in this population. We can postulate, however, and draw some conclusions from current data, which suggest that the risk/benefit ratio is similar to that for the non-diabetic population. Based on present information, postmenopausal diabetic women should be actively considered for HRT provided the physician is aware of the possible problems and the patient is sufficiently counselled to make an informed decision.
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PMID:Should women with diabetes mellitus receive hormone replacement therapy? 948 89

Many efforts have been made to trace the causes of Alzheimer's disease (AD). There are, however, many points of controversy among reports from the same country as well as among reports from different countries. The current study is a case-control study to determine the risk factors in the development of AD in Greece. Sixty-five patients with AD and 69 age-matched controls were examined. All patients with AD fulfilled the DSM-IV criteria for AD and NINCDS-ADRDA criteria for probable AD. Demographic characteristics such as gender, current marital status, who he/she is living with, education, main place of residence in childhood, adulthood, and late life, occupational hazards, patient's medical history (history of diabetes mellitus and hypertension), life habits like alcohol consumption and smoking, and a history of head trauma, heart attack, stroke, parkinsonism, or depression were collected from the subject or from an informant. A family history of selected diseases (hypertension, diabetes mellitus, dementia, Parkinson's disease, Down's syndrome, stroke) was also elicited. Ages of father and mother at birth were also recorded. Chi-square test, Kruskal-Wallis analysis of variance, cluster analysis, and logistic regression analysis were used for statistical analysis. The results (chi-square test) showed a statistically significant difference between patients with dementia of the Alzheimer type and controls as far as marital status (p = .04), the subject's history of major depressive episode (p = .02), and family history of dementia (p = .002) were concerned. Logistic regression analysis results produced a complex model of family aggregation of dementia, with patients with a history of depression and family history of dementia having an up to seven times higher risk of developing AD. These findings, especially a family history of dementia, are consistent with most of the literature.
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PMID:Risk factors for clinically diagnosed Alzheimer's disease: a case-control study of a Greek population. 951 31

In the literature the beneficial effects on health of drinking alcoholic beverages, especially red wine, is becoming increasingly more evident. We report an objective analysis of the advantages and the dangers of such a tendency. It appears that the daily consumption of red wine at moderate doses (200-400 ml a day) has real prophylactic effects. These are particularly marked in the prevention of coronary heart disease (CHD), but also for a possible cancer chemopreventive activity, in the prevention of type II diabetes, of ischemic stroke, of osteoporosis in older women, and of Alzheimer's disease. But, inasmuch as the consumption of alcoholic beverages always involves a potential danger (organic diseases, risk of dependence, alcoholism), from a medical point of view eulogy to wine is ethically indefensible. Similar effects may be obtained from a diet rich in fruits and fresh vegetables.
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PMID:[Eulogy of wine?]. 953 99

The two most common causes of vascular dementia (VAD) are dementia evolving in connection with multiple small or large strokes and dementia related to ischemic white-matter lesions (WMLs) of the brain. The knowledge about risk factors for these disorders is still scarce. Besides sharing risk factors with stroke, dementia with multiple small or large brain infarcts is also associated with non-vascular risk factors such as high alcohol consumption, psychological stress in early life, lower formal education, blue collar occupation, and occupational exposures. Risk factors for dementia in stroke victims include stroke-related and non-stroke related risk factors. Non-stroke-related factors are similar to those found in Alzheimer's disease. The main risk factors for ischemic WMLs are hypertension or increased blood pressure, but WMLs have also been associated with a number of other vascular risk factors. In recent years, Alzheimer's disease (AD) has also been reported to be associated with vascular risk factors, including hypertension, coronary heart disease, atrial fibrillation, diabetes mellitus, and WMLs. Although these associations may reflect an overdiagnosis of AD in cases with silent cerebrovascular disease, or that cerebrovascular disease increases the possibility that individuals with Alzheimer lesions will express a dementia syndrome, there are also alternative explanations. AD and cerebrovascular disease may for instance share similar risk factors or etiologic pathways. The pathogenetic implications for the association between AD and vascular factors need to be further explored. There is also a need for more studies on risk factors for VAD and risk factors for dementia in stroke samples, as well as studies on non-vascular risk factors for ischemic WMLs.
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PMID:Status of risk factors for vascular dementia. 954 18

There are seven centres for clinical genetics in the Netherlands. In 1996, some 63,000 persons (patients and possible carriers of hereditary diseases) were tested. In centres for clinical genetics chromosomal studies, biochemical diagnostics of hereditary metabolic diseases and DNA diagnostics are integrated with genetic counseling and prenatal diagnosis. The borders between the three different forms of laboratory testing for congenital anomalies and hereditary diseases gradually diminish. The variations of the numbers of laboratory examinations, genetic advices and prenatal diagnoses over the last ten years show that there is no correlation between these activities and the method of funding. Owing to the low prevalence of the diseases involved, the total number of DNA diagnoses for monogenic diseases will not increase significantly. However, once genetic risk factors of diseases such as cancer, cardiovascular diseases, diabetes, asthma, rheumatism, some psychiatric disorders and Alzheimer dementia will have been mapped, DNA diagnostics will greatly expand and will have implications in a broad area of medicine.
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PMID:[Clinical genetics in The Netherlands. I. Organization, activities and laboratory diagnosis]. 955 57

The attention in genetic research is shifting from the determination' of (rare) monogenic disorders to identification of genetic risk factors for important diseases at adult age. Mapping of all man's 80,000-100,000 genes will also provide more insight into the gene polymorphisms and mutations that are associated with various types of cancer, certain cardiovascular diseases, diabetes and neurodegenerative disorders, including Alzheimer dementia. Apart from new diagnostic possibilities, the DNA techniques create new prospects for the study of the pathogenesis of diseases and the devising of new strategies for treatment. Examples are familial hypercholesterolaemia, diabetes, breast cancer and colorectal carcinoma.
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PMID:[Future developments in genetic research. I. Technological possibilities]. 955 44

Mitochondrial DNA mutations have been implicated in a great variety of diseases, including such common ones as diabetes, Parkinson's disease and Alzheimer's, but the pathophysiological pathway leading from a specific mutation to a specific phenotype has remained elusive. Individuals with the same mutation can fall along a clinical spectrum ranging from asymptomatic to severely affected, and can even have completely different diseases. Much of this phenotypic heterogeneity has been attributed to the heteroplasmic nature of mitochondrial mutations, with both normal and mutated mitochondrial chromosomes being present in different proportions and tissue distributions. Isolated hearing loss is one of the only mitochondrial disorders that can be caused by homoplasmic mutations (e.g., only mutated mitochondrial mutations are present in all tissues). This review will outline the relationship between mitochondrial mutations and hearing loss while showing that even in a homoplasmic model, the two basic questions of mitochondrial genetics, penetrance and tissue specificity, remain unanswered: Why does the same mutation cause severe hearing loss in some family members but not in others, and why is the ear the only organ affected?
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PMID:Mitochondrial genetics and hearing loss: the missing link between genotype and phenotype. 957 47


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