Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002395 (Alzheimer's disease)
 110,584 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 78 carefully diagnosed dementia of Alzheimer type (DAT) patients, periodic synchronous discharges (PSD) on electroencephalograms (EEGs) were observed in 12 advanced cases. Although several case studies have been made since 1970, it is not widely recognized that PSD can be observed in advanced DAT patients. In this study the clinical picture, the nature of PSD, background activity of EEGs and 2 autopsied cases have been clinicopathologically investigated. The mean duration of the disease in the 12 cases was 6.7 years. The mean age of onset of the disease was 67 years of age. Among the 12 cases, 9 patients presented akinetic mutism or symptoms closely resembling akinetic mutism, who were completely bed-ridden with their extremities fixed in flexion. The other 3 patients were severely demented. They presented various degrees of Parkinsonian syndromes or paratonic rigidity accompanied by some infection and general fatigue. In one of these 3 patients, PSD were observed during the transient apallic state and the PSD themselves were also transient. The basic rhythm in EEGs were 4-6 c/s: middle amplitude theta waves dominant with delta waves on frontal leads. Triphasic delta, theta and sharp waves of PSD were dominant on centro-parieto-occipital leads. Background activity was not suppressed differing from that of Creutzfeld Jacob disease (CJD). According to the interval histograms of PSD, the majority presented an interval of 1-2 s (1.5 s mean) with some lability which was relatively slower than that of CJD. Fronto-parieto-occipital delay was not observed. By 1 c/s photic stimulation, PSD was not driven.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical and pathological evaluation of periodic synchronous discharge observed in advanced dementia of Alzheimer type]. 232 77

A structured interview covering the DSM-III criteria for major depression was adapted for separate use with Alzheimer's disease patients and with their families. Data from 36 patients yielded a depression rate of 13.9%, whereas information from their families indicated that the rate was 50.0%. This disagreement reflected greater family endorsement of patients' loss of interest or pleasure, irritability, fatigue, and feelings of worthlessness. Use of DSM-III-R criteria narrowed but did not eliminate the discrepancy between patients' and families' assessments of the patients' depression. Uniform procedures for gathering and integrating data from the family that are relevant to diagnosis in this group are indicated.
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PMID:Differences between patient and family assessments of depression in Alzheimer's disease. 230 71

The frequency of symptoms of depression (Feighner criteria) was evaluated in subjects with dementia of the Alzheimer type (DAT) and matched controls enrolled in a longitudinal natural history study of DAT. Despite enrollment criteria which excluded subjects with affective disorders, the collateral sources of subjects with DAT described these subjects as having significantly more "depressive" symptoms than controls without dementia at entry, and at 15- and 34-month follow-up. The collateral sources of the subjects with DAT reported that these demented individuals experienced significantly greater loss of interest, decreased energy, difficulty in thinking and concentrating, and psychomotor agitation or retardation then did the control group. The subjects with DAT reported fewer symptoms than did their collateral sources, but like their collateral sources, they did not report a global elevation of all Feighner symptoms, but rather related significantly greater difficulty in thinking and concentrating than the controls and a tendency toward loss of interest and psychomotor changes. No subject became clinically depressed. The results suggest a significant overlap between the symptoms of dementia and depression. The frequency with which the above symptoms occur in DAT confounds the use of Feighner and, by extension, DSM-III criteria in diagnosing depression in cognitively impaired individuals with DAT.
Alzheimer Dis Assoc Disord 1988
PMID:Symptoms of "depression" in dementia of the Alzheimer type. 319 69

To compare the efficacy and side effects of haloperidol and thioridazine in the management of behavioral symptoms of senile dementia of the Alzheimer's type, 16 patients were studied in an open crossover design study. Following 2-week drug washout, patients were alternately assigned to either haloperidol (1, 2, and 5 mg/day for 2 weeks) or thioridazine (25, 50, and 75 mg/day for 2 weeks). After completing the first neuroleptic, patients were washed out and then tried on the second neuroleptic. Six patients completed the crossover design, 1 received only haloperidol, and 9 received only thioridazine. Both drugs were effective in managing target behaviors, which included hostility, uncooperativeness, bothersomeness, emotional lability, and irritability. Complaints of fatigue and extrapyramidal side effects were greater with haloperidol than with thioridazine. Neither compound produced significant impairments in cognition as assessed by the Mini-Mental State Examination score or caused orthostatic hypertension.
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PMID:Haloperidol versus thioridazine in the treatment of behavioral symptoms in senile dementia of the Alzheimer's type: preliminary findings. 371 Oct 28

The complaints of 400 patients who were sent by their general practitioners to our hospital are enumerated in table 1 according to thier frequency (33 items). Three groups of complaints stand out: a) disturbances of memory and concentration b) nervousness - inward restlessness - increased irritability c) fatigue - decrease of performance. In the earlier literature similar syndromes were described as signs of the diminution of cerebral performance. If they appeared in old persons they were considered as an expression of a (physio-logical?) decrease of neurons. In middle-aged men the same syndrome was considered as sign of a premature cerebral arteriosclerosis. Recent investigations have shown that a decrease of cerebral performance is often due to a degenerative process of Alzheimer's type. In many cases it is difficult to decide concerning which of the three basic processes we have to take into consideration if a diminution in cerebral performance occurs. Presented are: Cues for diagnosis, differential diagnosis and treatment of the syndrome often seen in general practice today.
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PMID:[So-called presclerosis (developing cerebral ischemia)]. 724 33

There is growing evidence that the amyloid beta-peptide (beta 1-40) is involved in the aetiology of Alzheimer's disease also implicating an altered calcium homeostasis of affected cells. Beta 1-40 has been proposed to form calcium channels in synthetic bilayer membranes [1]. We wanted to investigate in the present study whether beta 1-40 (or fragments thereof) could act as ionophores in a biological membrane like the one in human erythrocytes. Incubation of the cells for 2 h and 4 h at 37 degrees C together with 6 mumol L-1 of beta 1-40 or of fragments beta 1-28 and beta 25-35, resulted in a significantly decreased energy charge qualitatively similar to the one obtained by a known calcium ionophore (A 23187, 0.05 mumol L-1). Moreover, beta 1-40 and its two fragments induced a significant alteration of 45Ca permeability in human red blood cells of the same type as the one achieved by the calcium ionophore. The ionophoric action of beta 1-40 and its two fragments may lead to an increase of the intracellular calcium ion concentration, in turn resulting in enhanced Ca(2+)-ATPase activity and a decrease in energy charge. This may be valid also for neuronal plasma membranes and could, therefore, be a possible aetiological mechanism in Alzheimer's disease.
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PMID:Alzheimer amyloid beta-peptides exhibit ionophore-like properties in human erythrocytes. 755 64

During the past 2 decades, great advances have been made in the treatment of ulcer disease. This has involved the development of new drugs that are not only well tolerated, but are relatively inexpensive. The lack of significant adverse effects has revealed a degree of tolerability that, to write a review of the adverse effects, poses a difficult task. Most of the adverse effects are related to an excessive reaction to the relevant pharmacological characteristic that mediates the therapeutic response. The drug dosage can be reduced, freeing the patient of the adverse reaction, but leaving behind a background activity adequate to produce a therapeutically beneficial effect. The adverse effects of H2-antagonists fall into 2 groups. Firstly, there are poorly defined symptoms that have a prevalence similar to that in the community; these include headache, giddiness, dizziness, fatigue, constipation and diarrhoea. Secondly, they may delay the metabolism of drugs metabolised by the the cytochrome P450 system, and rarely be androgenic. Many antacids and the site-protective agent sucralfate contain aluminium, which can be absorbed, producing elevation of serum aluminium levels. In view of the possible association of aluminium with Alzheimer's disease, anxiety has arisen as to whether aluminium from these sources may, in those on prolonged treatment, cause Alzheimer's disease. However, the evidence so far indicates that aluminium is not a risk factor for Alzheimer's disease. The association of gastric cancer with achlorhydria has led to the fear that long term use of potent acid inhibitors may cause cancer. This fear has been accentuated by the observation that some rats, given omeprazole over their lifetime, developed carcinoid tumours of the stomach. However, enthusiastic research, both clinical and epidemiological, indicates that drug-induced achlorhydria is unlikely to be a problem in humans. Site protective agents have a role in certain conditions such as pregnancy where the systemic effect of a drug may produce adverse effects.
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PMID:A comparative overview of the adverse effects of antiulcer drugs. 776 37

1. Family-provided care of members with Alzheimer's disease and related disorders (ADRD) is complicated by the presence of secondary behavioral symptoms, such as agitation, that lead to caregiver depression, burden, and breakdown. 2. Caregiver education to manage secondary symptoms in ADRD can be simplified by using a theoretical framework of person-environment fit, providing a selection of interventions to modify the environment to reduce demand on the dwindling resources of the demented person. 3. The Progressively Lowered Stress Threshold (PLST) model identifies six areas of stress for persons with ADRD fatigue, change of caregiver, environment or routine, demands to achieve beyond capability, multiple and competing stimuli, affective response to perceived losses, and physical stressors.
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PMID:Standardized care plan. Managing Alzheimer's patients at home. 785 17

Psychomotor stimulant drugs such as caffeine, nicotine, amphetamine and cocaine, have been shown to improve vigilance in man under conditions of fatigue. Nicotine has also been shown to improve performance in some cognitive tests in patients with Alzheimer's disease. In rodents these drugs increase activity which may confound "performance enhancing effects" in rodent models. However, improvements have been found in a number of tests that do not seem to be directly dependent upon an enhancement of locomotor activation. In one example, Evenden and Robbins (1985) reported consistent improvements in a visual tracking test following amphetamine. The present study was undertaken to determine whether these performance enhancing effects of amphetamine could also be obtained with cocaine and apomorphine, which both have psychomotor stimulant effects through their actions as, respectively, indirect and direct dopamine agonists, and by caffeine and nicotine, which do not have a direct dopaminergic mechanism of action. The results of the study indicate that all five drugs improved tracking performance at one or more doses. The most consistent effects were obtained with amphetamine which, like cocaine and nicotine, improved tracking at a dose which did not produce other changes in behaviour. Taking into account previous studies (Evenden and Robbins 1983, 1985), these results were interpreted as indicating that psychomotor stimulant drugs produce a general activation of behaviour. At all but the highest doses of such drugs, the form of behaviour that is observed depends upon the environment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caffeine and nicotine improve visual tracking by rats: a comparison with amphetamine, cocaine and apomorphine. 787 Aug 79

In this article we present evidence supporting the interaction between excitotoxicity, beta APP mismetabolism, metabolic compromise and intracellular calcium destabilization in the process of neurodegeneration associated with Alzheimer's disease (AD). AD is characterized by the presence of neurofibrillary tangles and amyloid-containing plaques in specific regions of the brain. There appear to be several processes which contribute to the neurodegeneration associated with AD. Although AD has been linked to genetic mutations on chromosomes 21, 19 and 14, there are sporadic forms of AD that have no known genetic mutation involved. Aging is the major risk factor for AD. During the course of normal aging several metabolic compromises may occur in the brain. Both decreased glucose transport and utilization, and increased glucocorticoid levels are known to occur with aging and may lead to decreased energy supplies, ATP depletion, failure of Ca2+ buffering systems, excess glutamate release and activation of glutamate receptors. In addition, a reduction in antioxidant enzymes and consequently an increase in free radicals has also been associated with aging. Each of the preceeding alterations would lead to an increase in neuronal [Ca2+]i. Elevated calcium could then activate calcium-dependent proteases which degrade particular cytoskeletal proteins, and lipases which generate free radicals resulting in membrane damage and possible cell death. In this article we provide evidence that amyloid beta-peptide (A beta), the substance which accumulates in AD plaques, exacerbates excitotoxic and metabolic compromises to neurons resulting in changes in the cytoskeleton which resemble those seen in the neurofibrillary tangles of AD. We also provide evidence that secreted forms of beta-amyloid precursor protein (beta APP) are neuroprotective against excitotoxic insults. Recent findings concerning the normal function of beta APP and the mechanism of A beta toxicity place beta APP at the center of changes leading to neuronal degeneration in AD.
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PMID:Glutamate, beta-amyloid precursor proteins, and calcium mediated neurofibrillary degeneration. 789 98


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