PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “BRAIN DISEASE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed2002

Hyponatremia in acute brain disease: the cerebral salt wasting syndrome.

Hyponatremia in acute brain disease is a common occurrence, especially after an aneurysmal subarachnoid hemorrhage. Originally, excessive natriuresis, called cerebral salt wasting, and later the syndrome of inappropriate antidiuretic hormone secretion (SIADH), were considered to be the causes of hyponatremia. In recent years, it has become clear that most of these patients are volume-depleted and have a negative sodium balance, consistent with the original description of cerebral salt wasting. Elevated plasma concentrations of atrial or brain natriuretic peptide have been identified as the putative natriuretic factor. Hyponatremia and volume depletion may aggravate neurological symptoms, and timely treatment with adequate replacement of water and NaCl is essential. The use of fludrocortisone to increase sodium reabsorption by the renal tubules may be an alternative approach.

Journal Article↗
PubMedDate not supplied

[Sensitivity of atherosclerosis indices in patients with ischemic brain disease].

Epidemiological studies suggest that dyslipoproteinemias and hyperlipoproteinemias present one of the most important risk factors in the development of atherosclerosis and its complications. The aim of this study was to find out which of the lipid status disorders in patients with ischemic brain disease was the most important risk factor in the development of cerebral atherosclerosis. Patients with ischemic brain disease were examined in the acute and subacute phase. Total blood cholesterol, low density lipoproteins (LDL) and high density lipoproteins (HDL) as well as of apolipoproteins A1 and B were determined. Correlations (atherogenic indices) of some lipid components with the severity of clinical course and echo-angiographic finding were determined. It was concluded that the highest correlation with the cerebral atherosclerosis severity degree existed with the level of apoA1 and apoB apolipoproteins, followed by correlation of LDL and HDL cholesterol, and the lowest correlation was found between HDL and the total cholesterol. Accordingly, apolipoproteins, i.e., apoA1/apoB indices are the most sensitive markers of the risk for atherogenesis.

Apolipoproteins↗
PubMed2000

Glutamine synthetase, hemoglobin alpha-chain, and macrophage migration inhibitory factor binding to amyloid beta-protein: their identification in rat brain by a novel affinity chromatography and in Alzheimer's disease brain by immunoprecipitation.

Proteins binding to amyloid beta-protein (Abeta) may modulate the accumulation of Abeta in Alzheimer's disease (AD) brain. We developed a monomeric Abeta column for isolation of the proteins binding to Abeta from rat brain. By amino acid sequence analysis and immunoreactivity with specific antibodies, we identified three new Abeta-binding proteins, glutamine synthetase, hemoglobin alpha-chain, and macrophage migration inhibitory factor as well as serum albumin, beta-tubulin, and glyceraldehyde-3-phosphate dehydrogenase already identified as proteins bound to amyloid beta-protein precursor. In addition, the retained fraction contained both apolipoprotein E and alpha(1)-antichymotrypsin already known as Abeta binding proteins. Furthermore, we detected the complexes of these new binding proteins with Abeta in a soluble fraction of the cerebral cortex of AD brain by immunoprecipitation. Our results suggest that these binding proteins also associate with Abeta, leading to the clearance or the accumulation of Abeta and the neuronal cell damage in human brain.

Alzheimer Disease↗
PubMed1981

Long-term intracellular retention of hexosaminidase A by Tay-Sachs disease brain and lung cells in vitro.

Enzyme-replacement treatment for metabolic storage disorders has been widely studied using model cell culture systems. This study determines the long-term fate of human hexosaminidase A supplied to Tay-Sachs disease brain and lung cells. Hex A retention studies showed that the incorporated Hex A is retained in undiminished quantity by TSD lung cells maintained in stationary culture for 14 days. Tay-Sachs disease brain cells similarly followed for 28 days in stationary culture showed an initial reduction in Hex A for 3 days, after which the Hex A level stabilized and remained relatively constant for the next 25 days. Hexosaminidase B isoenzyme was found to accumulate in both cell lines during extended cultivation, despite the observation that significant amounts were excreted into the extracellular environment. The demonstration of long-term intracellular retention of exogenously supplied therapeutic enzyme by the target cells offers additional evidence for the feasibility of an enzyme-replacement approach for study and treatment of lysosomal storage disorders.

Brain↗
PubMed1999

Cerebrovascular risk factors and depression in older primary care patients: testing a vascular brain disease model of depression.

The authors examined whether cerebrovascular risk factors (CVRFs) are associated with depressive diagnoses and symptoms in 303 primary-care patients age >/=60 years, as would be consistent with a small-vessel brain disease model of later-life depression. CVRFs were not significantly independently associated with major, minor, or subsyndromal depression, late-onset major depression, or overall depressive symptom severity. These data did not support the notion that a small-vessel brain disease model of depression might apply to the majority of older persons with depressive symptoms and syndromes in primary-care settings. Future work should include longitudinal study with larger sample sizes.

Aged↗
PubMed1975

Visual perception of line direction in patients with unilateral brain disease.

The accuracy of identifying the slope of briefly exposed lines was assessed in patients with lesions of the left or right hemisphere and in a group of control patients without history or evidence of brain disease. The frequency of impaired performance was remarkably high in the patients with right hemisphere lesions. In contrast, the patients with left hemisphere lesions did not perform differently from the control group. Visual field defect, aphasic disorder, and age were not related to performance level. The striking interhemispheric difference in performance on this visuospatial task suggests its further development for clinicodiagnostic purposes.

Adult↗
PubMedDate not supplied

Effects of estrogen on congnition mood, and degenerative brain diseases.

OBJECTIVE: To review research findings on the effects of estrogen on cognition, mood, memory, and degenerative brain disease in women. DATA SOURCES: English-language journal articles published primarily since 1995, retrieved from a MEDLINE search and from bibliographies of selected reviews. STUDY SELECTION: Investigational studies, clinical trials, and review articles examining the effects of estrogen on the central nervous system. DATA SYNTHESIS: Although scientific study of the brain is in its infancy, numerous studies indicate that estrogen is essential to optimal brain function. Estrogen has been shown to increase cerebral blood flow, act as an antiinflammatory agent, enhance activity at neuronal synapses, and exert direct neuroprotective and neurotrophic effects on brain tissue. Through these varied mechanisms, estrogen strongly influences mood and cognition, and the decline of this hormone at menopause can produce significant emotional and cognitive problems in women. CONCLUSION: Pharmacists can educate women about the various mood and memory changes that can occur during perimenopause and how estrogen replacement therapy may lead to improvements in brain function. The potential use of estrogen replacement therapy to reduce the risk of Alzheimer's disease and ease the symptoms of Parkinson's disease could have a profound effect on women, their families, and society as a whole.

Alzheimer Disease↗
PubMed1997

Addiction is a brain disease, and it matters.

Scientific advances over the past 20 years have shown that drug addiction is a chronic, relapsing disease that results from the prolonged effects of drugs on the brain. As with many other brain diseases, addiction has embedded behavioral and social-context aspects that are important parts of the disorder itself. Therefore, the most effective treatment approaches will include biological, behavioral, and social-context components. Recognizing addiction as a chronic, relapsing brain disorder characterized by compulsive drug seeking and use can impact society's overall health and social policy strategies and help diminish the health and social costs associated with drug abuse and addiction.

Behavior, Addictive↗