Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten affected individuals are described from a kindred with autosomal dominant familial Alzheimer's disease in which a mutation in the amyloid precursor protein gene results in a valine to glycine substitution at amyloid precursor protein 717 which co-segregates with the disease. The mean age at onset of symptoms was 52 years with a range from 40 years to 67 years. The median duration of the disease was 11 years, with a range of 7-16 years. All individuals fulfilled the National Institute for Neurological and Communicative Disorders and Stroke criteria for probable Alzheimer's disease. A homogeneous clinical and neuropsychological pattern was evident within the family. Myoclonic jerks, seizures, depression and a lack of insight were common features. Positron emission tomography demonstrated biparietal bitemporal hypometabolism in the one affected individual who was studied. The diagnosis was confirmed histopathologically in one individual.
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PMID:Familial Alzheimer's disease. A pedigree with a mis-sense mutation in the amyloid precursor protein gene (amyloid precursor protein 717 valine-->glycine). 846 68

Since 1984, there has been a great interest in the phenomenon of a particular seasonally recurrent mood disorder called seasonal affective disorder (SAD) or winter depression and its treatment: the phototherapy. Seasonal affective disorder is a syndrome described by Rosenthal in 1984. This mood disorder is characterized by depression with onset recurrent in autumn or winter and spontaneous spring or summer remission. It is associated with hypersomnia, anergia, increased appetite, weight gain and carbohydrate craving. The population prevalence in the north of the USA is estimated between 3 and 5%, but it changes with sex, age and also latitude. A long time ago, we know that animals are photoperiod sensitive and that the melatonin secretion in mammals is suppressed by the light. In 1980, Czeiler reported for the first time that human melatonin secretion can be suppressed by high light exposure (+/- 1500 lux). In 1982, Rosenthal, Lewy and al. reported an antidepressant effect of light exposure of a manic-depressive patient. The phototherapy was born. To treat the SAD, the most common procedure of phototherapy is to expose the subject during 2 hours early in the morning, between 06:00 and 09:00 AM. The subject is sitting before a light screen, he can work and has to fix the screen one time every minute. The most common side effects are headache, eyestrain, muscle pain. The ocular phototoxicity is controversed and it seems to be potentially dangerous if phototherapy is associated with tricyclic antidepressants, neuroleptics and other medication containing a tricyclic, heterocyclic or porphyrin ring system. Since this finding, many questions are asked about photoperiod and its effects in the human being. Lewy proposes for the winter depression the hypothesis of a phase delayed circadian rhythm, that can be treated by a morning light exposure. At the present time, many trials are going on to study the effects of phototherapy in other problems like insomnia, maladaptation to night work, jet lag and Alzheimer disease.
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PMID:[Seasonal affective syndrome and phototherapy: theoretical concepts and clinical applications]. 868 79

In this study, we have evaluated the levels of blood histamine, serum interleukin-1 beta (IL-1 beta), and plasma tumor necrosis factor-alpha (TNF-alpha) in 20 patients with mild to moderate Alzheimer disease (AD; 13 early onset and 7 late-onset AD subjects) and in 20 age-matched control subjects (C). AD patients showed higher concentrations of histamine (AD = 452.9 +/- 237.9 pmol/mL; C = 275.3 +/- 151.5 pmol/mL; p < 0.05) and IL-1 beta (AD = 211.2 +/- 31.1 pg/mL; C = 183.4 +/- 24.4 pg/mL; p < 0.01), and lower values of TNF-alpha (AD = 3.59 +/- 2.02 pg/mL; C = 9.47 +/- 2.64 pg/mL; p < 0.001) than elderly controls. Increased levels of histamine and decreased levels of TNF-alpha were observed in both early onset AD (EOAD) and late-onset AD (LOAD) patients, but only EOAD subjects had elevated serum IL-1 beta values compared with age-matched controls. Age negatively correlated with histamine (r = -0.57; p < 0.05) and positively with IL-1 beta levels (r = 0.48; p < 0.05) in healthy subjects, but not in AD, whereas a positive correlation between TNF-alpha scores and age was only found in AD patients (r = 0.46; p < 0.05). Furthermore, histamine and TNF-alpha values correlated negatively in AD (r = -0.50, p < 0.05). In addition, cognitive impairment increased in patients with lower TNF-alpha and higher histamine and IL-1 beta levels, as indicated by the correlations between mental performance scores and histamine (r = -0.37, ns), IL-1 beta (r = -0.33, ns) and TNF-alpha levels (r = 0.42, p < 0.05). Finally, histamine concentrations decreased as depression scores increased in AD (r = -0.63, p < 0.01). These data suggest a dysfunction in cytokine and histamine regulation in AD, probably indicating changes associated with inflammatory processes.
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PMID:Blood levels of histamine, IL-1 beta, and TNF-alpha in patients with mild to moderate Alzheimer disease. 897 99

The secreted form of beta-amyloid precursor protein (sAPP alpha) is released from neurons in an activity-dependent manner, and has been reported to modulate neuronal excitability in dissociated hippocampal neurons. We now report that sAPP alpha shifts the frequency dependence for induction of long-term depression of synaptic transmission (LTD) in hippocampal slices from adult rats. Whereas low frequency stimulation (1 Hz) of Schaffer collateral axons induced LTD of the post-synaptic response of CA1 neurons in control slices, it did not induce LTD in slices pretreated with sAPP alpha. On the other hand, whereas a 10 Hz stimulation normally induced neither LTD or LTP, it did induce LTD in slices pretreated with sAPP alpha. sAPP alpha potentiated LTP induced by high frequency stimulation. sAPP alpha induced cGMP production in hippocampal slices, and pretreatment of slices with 8-bromo-cyclic GMP mimicked the effect of sAPP alpha on LTD suggesting a role for cyclic GMP in modulation of LTD. The data suggest an important role for sAPP alpha in modulation of synaptic plasticity in the hippocampus.
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PMID:Secreted form of beta-amyloid precursor protein shifts the frequency dependency for induction of LTD, and enhances LTP in hippocampal slices. 924 98

Mutations in the presenilin-1 (PS-1) gene account for approximately 50% of the cases of autosomal dominant, early onset, inherited forms of Alzheimer's disease (AD). PS-1 is an integral membrane protein expressed in neurons and is localized primarily in the endoplasmic reticulum (ER). PS-1 mutations may promote neuronal degeneration by altering the processing of the beta-amyloid precursor protein (APP) and/or by engaging apoptotic pathways. Alternative processing of APP in AD may increase production of neurotoxic amyloid beta-peptide (Abeta) and reduce production of the neuroprotective alpha-secretase-derived form of APP (sAPPalpha). In differentiated PC12 cells expressing an AD-linked PS-1 mutation (L286V), sAPPalpha activated the transcription factor NF-kappaB and prevented apoptosis induced by Abeta. Treatment of cells with kappaB decoy DNA blocked the antiapoptotic action of sAPPalpha, demonstrating the requirement for NF-kappaB activation in the cytoprotective action of sAPPalpha. Cells expressing mutant PS-1 exhibited an aberrant pattern of NF-kappaB activity following exposure to Abeta, which was characterized by enhanced early activation of NF-kappaB followed by a prolonged depression of activity. Blockade of NF-kappaB activity in cells expressing mutant PS-1 by kappaB decoy DNA was associated with enhanced Abeta-induced increases of [Ca2+]i and mitochondrial dysfunction. Treatment of cells with sAPPalpha stabilized [Ca2+]i and mitochondrial function and suppressed oxidative stress by a mechanism involving activation of NF-kappaB. Blockade of ER calcium release prevented (and stimulation of ER calcium release by thapsigargin induced) apoptosis in cells expressing mutant PS-1, suggesting a pivotal role for ER calcium release in the proapoptotic action of mutant PS-1. Finally, a role for NF-kappaB in preventing apoptosis induced by ER calcium release was demonstrated by data showing that sAPPalpha prevents thapsigargin-induced apoptosis, an effect blocked by kappaB decoy DNA. We conclude that sAPPalpha stabilizes cellular calcium homeostasis and protects neural cells against the proapoptotic action of mutant PS-1 by a mechanism involving activation of NF-kappaB. The data further suggest that PS-1 mutations result in aberrant NF-kappaB regulation that may render neurons vulnerable to apoptosis.
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PMID:Secreted beta-amyloid precursor protein counteracts the proapoptotic action of mutant presenilin-1 by activation of NF-kappaB and stabilization of calcium homeostasis. 957 87

Today, pseudodementia seems to be a blurred and misleading term. It is more precise to speak about cognitive disorders which can be observed in both depressed and demented patients. Guidelines which can help to differentiate between depression and dementia are proposed for both the history and the course of the disorders. Additional brain imaging can give further indications. Ergopsychometric setting, which obeys directed burden under speed conditions may be helpful. SSRIs may reduce the HPA axis hyperactivity in depressive patients with Alzheimer disease. Therefore this medication can help to improve the state of these patients.
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PMID:Problems of differential diagnosis between depressive pseudodementia and Alzheimer's disease. 970 Jun 48

The purpose of this study was to investigate noncognitive symptoms in Alzheimer disease to identify symptom patterns and to study stability of such patterns prospectively. Furthermore, variables were examined that could be associated with certain types of symptom patterns or could be predictors of change of these patterns. Forty-eight patients with the clinical diagnosis of probable Alzheimer disease were included in this study and were assessed weekly over a 3-week period. Noncognitive symptoms were rated according to the Behavioral Abnormalities in Alzheimer's Disease Rating Scale and the Dementia Mood Assessment Scale and to a set of items that specifically assess misidentifications. By means of principal component factor analysis different noncognitive symptom patterns were obtained, yielding a four-factor solution. They mapped onto rational domains with respect to clinical experience: depression, apathy, psychotic symptoms/aggression, and misidentifications/agitation. Demographic and clinical variables were not associated with the factor solutions and did not predict change of the factor values. The results demonstrate that in Alzheimer disease there are distinct noncognitive symptom patterns that hold at least short-term prospective stability. None of the examined clinical variables, such as age at entry, the status of the patients (outpatient or inpatient), or dementia severity, exerted substantial influence on the noncognitive symptom patterns. Further investigations should concentrate on the pathological and prognostic correlates of noncognitive symptom patterns in Alzheimer disease.
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PMID:Presentation and stability of noncognitive symptom patterns in patients with Alzheimer disease. 987 60

The aim of the present study was to document behavioral disturbances in dementia patients in a sample not specifically referred to a clinic. Ninety patients with dementia in a community were studied in relation to the behavioral and psychiatric manifestations as perceived by their caregivers. They were categorized into two subgroups based on severity of the illness, namely mild and moderate-severe, for the purpose of comparison. There were 68 patients with Alzheimer disease, 10 with vascular dementia, and the remaining 12 formed a miscellaneous group.The frequency of the following behaviors in relation to the severity of the dementia were assessed: aggression, physical violence, wandering, incontinence, disinhibition, binge-eating, hallucinations, delusions, and depression. The most common behavioral change was aggression (59%), followed by wandering (27%), delusions (22%), and incontinence (18%). Aggression caused the most distress to the caregiver. There was a higher incidence of wandering, incontinence (p= 0.009), and persecutory delusions (p=0.02) in the moderate severe group. A significantly higher proportion of the moderate-severe group required further care and intervention (p=0.04). This study is probably one of the rare nonclinical surveys on this subject.
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PMID:Behavioral and psychiatric manifestations in dementia patients in a community: caregiver burden and outcome. 987 61

This study investigated the prevalence of depressive symptoms among White Hispanic (WH) and White non-Hispanic (WNH) first-degree family caregivers. We screened 653 primary caregivers of family members with possible or probable Alzheimer disease who presented at our outpatient memory disorders clinic. Caregiver depression was assessed utilizing the Center for Epidemiologic Studies-Depression (CES-D) Scale. Overall, depression (CES-D scores > or = 16) was more common among WH (45%) than among WNH (36%) caregivers (p < 0.05). Elevated CES-D scores among the entire caregiving sample were also linked with being a female spouse (p=0.002), increased level of patient cognitive impairment (p=0.002), and patient psychosis (p=0.002). Risk factors for caregiver depression were identified and compared when the sample was stratified by ethnicity (WH and WNH) and generation (spouses and children). Patient cognitive impairment was a predictor of caregiver depression only among WH spouses and children, whereas patient psychosis was a predictor only among WNH spouses. Female caregiver gender was the most robust risk factor for caregiver depression, being a predictor in all groups except WH children. Implications of this study include the need for increased clinical sensitivity to depression in ethnic minority caregivers, treatment of psychiatric morbidity in dementia caregivers, and respite care for caregivers with high risk for depression.
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PMID:Depressive symptomatology in first-degree family caregivers of Alzheimer disease patients: a cross-ethnic comparison. 987 63

In the article we discuss the role of serotonin in maintaining homeostasis paying special attention to the endocrinological aspect of the matter. It has been proved that it contributes to hypothalamus and hypophysis secretion regulation and interferes with paracrine activity in digestive and reproductive system. It is also an important constituent of platelets and takes part in aggregation and coagulation. It is known to be an atherogenic factor and to act as a growth stimulator for blood cells. It can be produced in exceed amounts by neoplasm or be released by activated thrombocytes during stress or coagulation. The influence of this hormone on the most of regulation mechanisms seems obvious. Presence of many different receptors as well as their number in all the structures of mammalian body makes it possible to use a range of agonists and antagonists in research concerning psychiatric diseases (e.g. bulimia, anorexia, depression), Alzheimer disease, migraine, hypertension, carcinoid related syndrome, multiple endocrine neoplasms and pre-menstrual syndrome. The promising results enable to use some of the modifiers in their clinical treatment though more research is needed for fully satisfactory effects.
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PMID:[Serotonin--structure, activity and clinical significance]. 1009 81


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