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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The characteristic morphologic changes frequently observed in the brain of an old adult include a decrease in weight and volume, a change in the pattern of cerebral cortical convolutions, and an increase in ventricular size. Cell loss varies from region to region in the brain, and may be intensified in Alzheimer's disease and other disorders associated with senile dementia. Among the neuroglial cells, the microglia undergo the most significant changes with age. Although senile brain disease previously has been regarded as secondary to atherosclerosis, recent neuropathologic studies indicate that only 30 to 40 percent of senile brain disease arises from cerebrovascular pathologic lesions. The dilemma remains, however, of how much of the deterioration observed in the aged is related to disease and how much to senescence. The interaction between gene expression and environmental conditions in aging is another important question for the geriatrician. Progress in the control and treatment of disorders associated with old age depends upon further research into the mechanisms that underlie the process of aging in the brain.
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PMID:How the human brain responds to aging. 17 40

A clinicoanatomical study was conducted in 218 cases of atherosclerotic dementia. 12 cases (5,5% of the total amount) showed diagnostic errors. Atherosclerotic dementia with Alzhemier-like symptomatology during life was considered to be Alzheimers disease, while Alzheimers disease, complicated by cerebral atherosclerosis as atherosclerotic dementia. Some objective and subjective factors of diagnostic errors were established. Late detection of such patients is considered as one of the risk factors of diagnostic errors during life.
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PMID:[Several diagnostic errors in cerebral atherosclerosis (clinico-anatomic study)]. 46 65

The paper is concerned with a study of confabulation seen in 95 patients. A gradual development of the confabulatory syndrome (from mnemonic confabulations to ecmnestic) was seen in senile dementia (5 cases) and in its combination with vascular atherosclerosis (61 cases). An acute development of confabulations (with a prevalence of mnemonic false reminiscence over ecmnestic) was seen in cerebral atherosclerosis (9 cases). Rudimentary ecmnestic confabulations, without mnemonic were seen in Alzheimer's disease (20 cases). The author established a certain correlation between ecmnestic confabulations and disturbances of fixation, between mnemonic confabulations and disorders of selective reproductivity, between their expressiveness and emotional liveliness and the degree of actualization of the past events. In a complacent-euphoric and anxiety affect the confabulations were spontaneous and were accompanied by psuedoactivity. In depressive states they were fragmentary and were detected only in response to questions. Aphatic disorders and the severity of dementia influence the mnestic confabulations making them poorer and incomplete.
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PMID:[Confabulation in atrophic and vascular disease of old age (clinico-psychopathologic findings)]. 97 23

Platelets seem involved in pathogenesis of atherosclerosis and Alzheimer disease which frequency increases with population ageing. Platelet hyperactivation may contribute to atherosclerosis by release of factors, which increase fibroblast and smooth muscle cell proliferation and perhaps lipid deposition. Many studies evidenced an increased platelet activation with ageing concomitantly to an increase of some coagulation factors, and an impaired response of endothelial cells leading to a prethrombotic state and facilitating the occurrence of atherosclerosis. On the other hand, in Alzheimer disease, a deposit of amyloid beta protein responsible for vascular and neuronal damage was evidenced. Platelet activation is responsible for the release of an amyloid beta protein precursor (the protease nexin 2). An increased platelet activation as demonstrated with aging, may thus explained the increased occurrence of Alzheimer disease.
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PMID:[Platelets and aging]. 149 75

The most important pathophysiological and pathogenetic facts are: The lower autoregulation threshold of cerebral blood flow and hypoxidosis, blood pressure in bradycardia, cerebral fits and stroke marks in CT, carotid atherosclerosis; reduced cerebral metabolism in chronic alcoholism and Wernicke. Reversible hypoglycemic induced hemiplegia. Multiinfarct syndrome and cerebral degenerative process Alzheimer. Effect of treatment by Piracetam.
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PMID:[Pathophysiology, clinical aspects and therapy of pre- and postoperative disorders of cerebral circulation and function]. 198 1

Analysis of the pathology of multi-infarct dementia is best carried out using a two-axis approach. The first axis describes the tissue damage, classified as macroinfarcts, cortical microinfarcts, basal ganglionic lacunes, white matter lacunes, dilated perivascular spaces, diffuse white matter rarefaction, and perivascular edema. The second axis describes the vascular abnormalities, classified as atherosclerosis involving the extracranial or intracranial arteries, arteriolosclerosis, congophilic angiopathy, emboli, and no structural abnormality. Multiple infarcts and white matter rarefaction are commonly seen as a component of Alzheimer disease, in keeping with the development of congophilic angiopathy and possibly other vascular changes in the latter disease. Evidence is presented to support the concept that the white matter rarefaction of Alzheimer disease and aging is associated with perivascular edema, rather than partial infarction.
Alzheimer Dis Assoc Disord 1991
PMID:The pathological basis of multi-infarct dementia. 205 11

Arteriolosclerotic leucoencephalopathy in the elderly (ALE) is characterized by white matter lesions associated with atherosclerosis and arteriolosclerosis. Mild lesions are focal and probably represent early status cribosus or incomplete lacunar infarcts. Moderate and severe lesions are diffuse areas of demyelination in the centrum semiovale in which lacunar infarcts are seldom observed. The incidence of ALE in a consecutive necropsy series of 50 cases (mean age 62.6 +/- 13.1 years) was 52%, it was rare in the fourth and fifth decades but increased thereafter to reach a prevalence of 100% at the age of 80 years. Mild lesions occurred in 19 patients and lesions were moderate or severe in 7 (14%). The mean age was higher in this group (74.7 +/- 7.6 years) than in patients with white matter changes as a whole. Dementia occurred only in 3 patients with moderate or severe ALE. These data suggest that (a) ALE is common in old age and is probably the cause of leuko-araiosis in most CT scans in the elderly; (b) ALE may be asymptomatic; (c) the severity of white matter changes may be not related to the severity of neurological deficits; and (d) multiple lacunar infarcts or associated degenerative diseases (i.e., Alzheimer's disease) may be the main cause of dementia in patients with ALE. White matter lesions in ALE, Binswanger's disease, transition areas in multi-infarct encephalopathy (MIE) and Alzheimer's disease (AD) are similar in morphology and are probably the result of a subacute hypoperfusion/hypoxic process. Increased arterial blood pressure is a frequent risk factor in ALE, Binswanger's disease and MIE, whereas congophilic angiopathy of the meningeal and cortical vessels, in addition to mild or moderate arteriolar hyalinosis in the white matter, may play a role in the pathogenesis of incomplete infarctation of the white matter in patients with AD.
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PMID:Arteriolosclerotic leucoencephalopathy in the elderly and its relation to white matter lesions in Binswanger's disease, multi-infarct encephalopathy and Alzheimer's disease. 223 Aug 30

The development of age pathology has been studied in relation to changes occurring in the activity of various genes and in the synthesis of various proteins as well as in relation to the topography of those changes. The relationship between age-related changes in the activity of various genes and the onset of atherosclerosis, cancer, diabetes, Parkinson's disease and Alzheimer's disease has been studied. The appearance of gene regulatory age-related changes in cells of the nervous, endocrine and immune systems determines their involvement in the age pathology development. The prospects of gene regulatory therapy aimed at selective activation and suppression of various gene groups are outlined.
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PMID:[Genoregulatory mechanisms of aging as a basis for the development of age-related pathology]. 227 89

Blood levels of triglycerides, total cholesterol, isolated lipoprotein fractions (VLDL-LDL- and HDL-cholesterol) and apoproteins (Apo-A1 and Apo-B) were examined in multi-infarct dementia, senile dementia of the Alzheimer type, ischemic stroke associated with carotid atherosclerosis and in control subjects. Forty patients divided into 10 consecutive patients for each group were studied. Alzheimer patients showed mean total cholesterol and Apo-B values significantly higher than control subjects. Apo-B was significantly higher in stroke patients than in controls. The mean lowest HDL-cholesterol (HDL-c) value was observed in stroke patients. No significant differences in mean HDL-c levels were found between patients with multi-infarct and Alzheimer dementia.
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PMID:Serum lipoprotein pattern variations in dementia and ischemic stroke. 233 Aug 21

Atherosclerosis and its relationship with mental disorders, in particular in advanced age, arouses vivid interest of specialists at home and abroad. In their paper the authors focused attention on the historical development of the term dementia in the work of European doctors, starting in the second century after Christ, on the genesis of the term atherosclerosis and some discoveries associated with disease. Special attention is devoted to circumstances of the nosological differentiation of atherosclerotic mental disorders. The authors emphasize the importance of Binswanger's and Alzheimer's work in this area and draw attention to progressive elements in the work of K. Kuffner.
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PMID:[The beginnings of the history of atherosclerosis in mental disorders]. 269 82


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