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At least 973 records · Page 54Linked to original sources
PubMed2005

Measuring treatment response in Alzheimer's disease clinical trials.

Alzheimer's disease (AD) is a progressive disorder that negatively impacts cognitive, behavioral, and functional abilities. Because of the complex nature of this disease, it is crucial to design assessment procedures that accurately track disease progression across a wide variety of symptom domains. One important use of such techniques is to assess the effectiveness of therapeutic compounds in AD clinical trials. A number of outcome measures that assess cognitive, behavioral, functional, or global ability have been developed for this purpose. This paper describes the assessment measures that are most commonly used in AD trials. The inherent strengths and limitations of each evaluative technique are summarized, as well as how these outcome measures are useful to the practicing clinician.

Activities of Daily Living↗
PubMed2005

Mild cognitive impairment and preclinical Alzheimer's disease.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by a gradual decline of numerous cognitive processes, culminating in dementia. Mild cognitive impairment (MCI) is a relatively broad clinical condition involving a slight memory deficit, which in many cases represents a transitional state between normal cognition and AD. Much research is currently being conducted on MCI, since any therapy that is effective at treating this early manifestation of dementia may provide an opportunity for managing the disease while patient function is relatively preserved. Current research seeks to develop disease-modifying treatments that intervene in the pathobiologic processes involved in MCI and AD. Another goal of current research is to develop antecedent biomarkers that can be used to detect AD prior to the appearance of symptoms and before substantial and irreversible brain damage occurs.

Activities of Daily Living↗
PubMed2005

Alzheimer's disease care management plan: maximizing patient care.

Nurse practitioners have the potential to significantly impact the care of patients with dementia. Healthcare providers can now offer patients medications that will control symptoms and prolong functioning. As a result of ongoing contact with patients, NPs play an important role in assessing and screening patients for AD and educating the patients, families, and caregivers about the disease. Alzheimer's disease is a chronic, progressive illness that requires long-term management. Nurse practitioners should be familiar with available medications and appreciate the need to individualize therapy to maximize efficacy and minimize potential adverse drug reactions.

Alzheimer Disease↗
PubMed2006

I remember.

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Aged↗
PubMed2006

[Open angle glaucoma: epidemiology, pathogenesis and prevention].

There is growing evidence that reactive oxygen species (ROS) play a key role in the pathogenesis of primary open angle glaucoma (POAG). The occurrence of oxidative DNA damage in trabecular meshwork (TM) has been demonstrated by measuring the increase of 8-hydroxy-2'-deoxyguanosine, the most abundant DNA oxidative alteration, which is significantly increased in glaucoma-bearing subjects as compared with unaffected controls. Several lines of evidence support the hypothesis that ROS play a fundamental pathogenic role, including the following: (a) outflow resistance in the anterior chamber increases in the presence of high levels of hydrogen peroxide; (b) TM possesses abundant antioxidant activities; (c) significant increases in superoxide dismutase and glutathione peroxidase activities were detected in the aqueous humour of glaucoma patients; (d) hydrogen peroxide compromises TM integrity. The existence of a significant correlation between oxidative DNA damage and intraocular pressure in glaucoma patients has been reported. POAG patients appear to have a genetic predisposition rendering them susceptible to ROS-induced damage because of a more frequent deletion, as compared to controls, of the gene encoding for glutathione-S-transferase M1, a pivotal anti-oxidant activity. Furthermore, oxidative stress, occurring not only in TM but also in retinal cells, appears to be involved in the neuronal cell death that characterizes POAG. These considerations could bear relevance for POAG prevention and suggest that genetic analyses and the use of drugs or dietary measures attenuating the effects of ROS, if validated in future studies, could be useful tools contributing to the control of this disease.

Adrenergic beta-Antagonists↗
PubMed2005

Dementia.

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Alzheimer Disease↗
PubMedDate not supplied

The effect of apomorphine, amantadine and dimethylaminoadamantane on the level of cyclic AMP in the rat striatum.

The content of cyclic AMP (cAMP) in the slices of rat striatum and cerebral cortex was tested after incubation with various concentrations (10(-6)--10(4) M) of dopamine (DA), apomorphine (APM), amantadine (AMD), and dimethylaminoadamatane (DMAD), and incubation with DA, AMD and DMAD in combination with KCl (43 mM) or haloperidol (HP) (10(-5) M). APM, AMD, and DMAD act synergistically with DA, elevate the c-AMP content in the striatum less than DA dose and do not affect the level c-AMP in the slices of cerebral cortex. KCl potentiated the action of DA, but inhibited that of APM, AMD, and DMAD. HP was most effective in blocking the action of DA, and blocked more weakly the action of APM AMD, DMAD, and the action of DA, APM, AMD, and DMAD in the presence of high concentration of KCl. The results indicate that APM, AMD, and DMAD, are less specific stimulants of central dopaminergic structures than DA, and that the increase of c-AMP content in the slices of rat striatum caused by APM, AMD, and DMAD is due to depolarizing action of these compounds.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

The effect of drugs stimulating central dopaminergic system on transformation of exogenous adenine into c-AMP.

We tested the effect of dopamine (DA), apomorphine (APM), amantadine (AMD), dimethylaminoadamantane (DMAD) or haloperidol (HP) on the in vitro formation of c-AMP from ATP labelled intracellularly with exogenous 14C-adenine or from endogenous ATP in the slices of rat striatum. DA stimulated the synthesis of c-AMP from endogenous and 14C-adenine labelled ATP. Nonspecific stimulants of the dopaminergic system, APM, AMD and DMAD, stimulated the c-AMP synthesis much weaker than DA did. After application of APM, ADM or DMAD, the utilization of ATP formed from 14C/U/adenine for synthesis of c-AMP was lower than after DA. The effects of combined treatment with DA together with APM, AMD or DMAD was additive. HP, 1 X 10(-3) M did not change the amount of radioactive and total c-AMP, but inhibited the stimulatory action of DA and, to a lesser degree, of APM, AMD and DMAD. The synthesis of c-AMP from endogenous ATP stimulated with APM, AMD and DMAD in striate body slices was inhibited by HP more strongly than the synthesis of c-AMP from ATP labelled with exogenous 14C-adenine. The results indicate that ATP synthesized from intracellular adenyl nucleotides is more effectively utilized for the synthesis of c-AMP stimulated by APM, AMD or DMAD in striate body slices, than ATP labelled with 14C-adenine.

Adenine↗
PubMedDate not supplied

The effect of agents stimulating dopaminergic system on incorporation of exogenous adenine into striate body slices of the rat.

We tested the effect of various concentrations (10(-6)--10(-4) M) of dopamine (DA), apomorphine (APM), amantadine (AMD), dimethylaminoadamantane (DMAD) and haloperidol (HP) on in vitro incorporation of 14C/U/adenine to slices of the rat striate body. Two mechanisms participated in this incorporation: one of them (uptake I) of Km = 1.92 micron, the second (uptake II) of Km 434 micron, APM inhibited both uptake I and II, while AMD and DMAD only the uptake I. HP at concentration inhibiting the dopaminergic receptors did not affect the inhibition by APM, AMD or DMAD of incorporation of exogenous adenine to striatal slices. Incorporation of exogenous adenine was not related to stimulation by specific (DA) or unspecific (APM, AMD, DMAD) stimulants of dopaminergic receptors in the rat striate body. The inhibition of the uptake produced by APM, AMD and DMAD may be related to the mechanism of action of these compounds.

Adenine↗
PubMed1997

Excitatory mechanisms in retinal ganglion cell death in primary open angle glaucoma (POAG).

Glaucoma is a leading cause of blindness worldwide and the second leading cause of irreversible blindness in the United States. The most common form of glaucoma, primary open angle glaucoma, is characterized by a chronically elevated intraocular pressure in the absence of any demonstrable structural abnormalities in the eye. The pathologic hallmark of glaucomatous optic neuropathy is the selective death of retinal ganglion cells, generally attributed to an elevated intraocular pressure. However, the histopathology of glaucomatous injury is strikingly similar to the pattern seen with the administration of toxic levels of glutamate. We have found that glaucoma is associated with elevated levels of intraocular glutamate-to a level toxic to ganglion cells. We propose that an elevation of vitreal glutamate may be responsible, at least in part, for the loss of ganglion cells seen in open angle glaucoma.

Animals↗
PubMed1976

Histofluorescence studies on the effect of 1,3-dimethyl-5-adamantanamine (D-145) on serotonin neurons in midbrain raphe nuclei.

1,3-Dimethyl-5-adamantanamine (D-145), a dopamine system stimulating agent, given at doses of 10-40 mg/kg ip, 2-5 hr before sacrifice, depressed the intensity of serotonin fluorescence in the rat midbrain raphe nuclei. Spiroperidol, 2 mg/kg ip, given 5 min before D-145, prevented the depression of serotonin fluorescence in the dorsal raphe nucleus (NDR), but not in the other groups of serotonin midbrain neurons. The results suggest a functional interaction between dopaminergic neurons and serotoninergic neurons in NDR.

Amantadine↗
PubMed1976

The influence of 1,3-dimethyl-5-adamantanamine (D-145) on catecholaminergic neurons of the rat brain, Histofluorescence studies.

The effect of a compound stimulating central dopaminergic structures, 1,3-dimethyl-5-adamantanamine (D-145), on the intensity of fluorescence in catecholaminergic nerve endings in some regions of the rat brain, mainly in the striatum and hypothalamus, was investigated with the modificated histofluorescence technique of Falck and Hillarp. D-145 (20 mg/kg), 2-3 hr after the administration depressed the intensity of catecholamine (CA) fluorescence in caudate-putamen (CP) and hypothalamic paraventricular nucleus (PVH). A blockade of dopamine (DA) receptors with spiperone (SPIRO, 2 mg/kg, 5 min before D-145) abolished the D-145 effect in PVH, thus indicating an indirect effect of D-145 on PVH, via a dopaminergic system. D-145 potentiated the depression of CA fluorescence produced by alpha-methyl-tyrosine methyl ester (H 44/68), 250 mg/kg ip. High doses of the CA synthesis inhibitor (2 X 400 mg/kg ip) prevented the developing of stimulation produced by D-145. These data indicate that the action of D-145 on DA receptors is indirect, via endogenous DA.

Amantadine↗