PubMed Health⌕ Search

Biomedical subjects

R J Branconnier

Publications and source records attributed to R J Branconnier.

At least 19 recordsLinked to original sources
PubMed1992

Blocking the Ca(2+)-activated cytotoxic mechanisms of cholinergic neuronal death: a novel treatment strategy for Alzheimer's disease.

The major neuropathological finding in Alzheimer's disease (AD) is the death of cholinergic cell bodies originating in the nucleus basalis of Mynert. This paper will review the data suggesting that a pharmacologic strategy designed to slow the rate of cholinergic neuronal death (CND) should be of palliative value in the treatment of AD. Recent data on the biology of cell death (CD) show that there are two patterns of CD: necrosis and apoptosis or genetically controlled, programmed cell death. Regardless of whether cells die by necrosis or apoptosis, four Ca(2+)-activated cytotoxic mechanisms are triggered. Cytosolic free [Ca2+]i increases with aging. After 75 years, this rise may lead to the activation of a putative apoptotic gene in AD that results in CND. Since the increase in cytosolic [Ca2+]i may be mediated by the voltage operated L-type Ca2+ channel on the neuronal cell body, chronic treatment with an L-channel blocker, like nimodipine, might palliate the progression of and possibly prevent the majority of cases of AD.

Alzheimer Disease↗
PubMed1984

Prediction of serum cortisol response to dexamethasone in normal volunteers: a multivariate approach.

Dexamethasone (DEX, 0.5 mg orally at 11 PM) challenge was used for the assessment of hypothalamic-pituitary-adrenal (HPA) activity in 20 normal volunteers. Age and pre-DEX serum cortisol levels were theè evaluated as predictors of postDEX serum cortisol levels using step-wise multiple regression analysis. Both age and preDEX serum cortisol levels were significant predictors of postDEX serum cortisol levels. It is suggested that the adjustment for age and preDEX serum cortisol level could be useful for the interpretation of abnormal postDEX levels.

Adolescent↗
PubMed1984

The effect of aging on the positive chronotropic response to amitriptyline.

Amitriptyline (AT) increases sinus heart rate (SHR) due to inhibition of the reuptake of norepinephrine in combination with an antimuscarinic blockade of cardiac vagal inhibition. After 150 mg/day AT for 28 days, the change in SHR was negatively correlated with age in 42 depressed patients who were 18-85 years of age. This finding is consistent with observations that the tachycardic response to antimuscarinics and catecholamines decreases with aging.

Adult↗
PubMed1983

[Neuropsychological study of decline of attention and drug therapy of patients with Alzheimer's disease].

The present study provided a neuropsychological assessment of impaired attention in Alzheimer's patients (57-89 years of age). Three control groups were evaluated: young normals (ages 18-32 years of age), an older group (55-69 years of age), and an elderly group (70-85 years of age). Alzheimer's patients showed an absence of CNV rebound and impairment in attention performance. They also showed significantly less facilitation in speed of response by a preparatory signal than the non-patient groups. These findings suggested a possible discontinuity between normal aging and Alzheimer's disease. On the other hand, a comparison of young, normal elderly, and Alzheimer's groups indicated a pattern of systematic decrease in CNV rebound, lowered short-term memory performance, and slowing of reaction time during divided-attention, a finding that suggests normal aging and senile dementia to represent quantitative differences on a continuum of gradual age-related deterioration. Alzheimer's patients showed elevated levels of basal heart rate and eyeblink rate and increased oculomotor responsiveness in divided-attention conditions. This finding was interpreted as compelling evidence against the concept of hypoactivity in senile dementia and as support for a distraction-arousal interpretation of impaired attention in Alzheimer's patients, although decreased basal myogenic activity and lowered heart rate levels during divided attention in the patients indicated selectively dampened psycho-physiological functioning. Distraction-arousal processes appeared to be curtailed in the patient group after Hydergine treatment.

Adult↗
PubMed1983

Aging and cortisol resistance to suppression by dexamethasone: a positive correlation.

Cortisol resistance to suppression by 0.5 mg of dexamethasone given at 11 p.m. was studied in 30 normal subjects, 17 to 78 years of age. Serum cortisol concentrations were determined by radioimmunoassay. A strong positive correlation was found between age and cortisol concentrations 9 hours after dexamethasone administration. The data suggest that aging, per se, might contribute to the increased cortisol resistance to suppression by dexamethasone reported in depression and dementia.

Adolescent↗
PubMed1983

Clinical pharmacology of bupropion and imipramine in elderly depressives.

The clinical efficacy and adverse reaction profile of bupropion, an atypical antidepressant, was compared with the tricyclic imipramine in 63 elderly depressives. Patients were randomly assigned to treatment with 150 or 450 mg/day of bupropion, 150 mg/day of imipramine, or placebo for 35 days. Both doses of bupropion were equivalent to imipramine in antidepressant efficacy. The higher dose of bupropion had a more rapid onset of effect than the low dose and significantly greater anxiolytic activity than either imipramine or the lower dose. Both doses of bupropion had adverse reaction profiles strikingly similar to placebo and, in marked contrast to imipramine, did not produce sedation or anticholinergic side effects. Cognition improved equally in all groups. It was concluded that bupropion has therapeutic advantages over the tricyclics in the treatment of elderly depressives.

Age Factors↗
PubMed1982

Amitriptyline selectively disrupts verbal recall from secondary memory of the normal aged.

Amitriptyline, a frequently prescribed tricyclic antidepressant, is reported to produce an age-related impairment in anterograde memory. However, the locus of this adverse effect has never been described within the context of contemporary learning and memory theory. Fifteen normal elderly subjects were treated with 50 mg amitriptyline and placebo in a cross-over study. A computerized stage analysis of memory revealed that sensory and primary memory were not affected while verbal recall from secondary memory was markedly disrupted by amitriptyline. Further examination of secondary memory revealed that amitriptyline impaired recall, but not recognition. The profile of anterograde memory impairments observed with amitriptyline is similar to that previously reported for the antimuscarinic, scopolamine. Since amitriptyline at the dose employed in this study would be expected to exert marked central antimuscarinic effects, it appears likely that it is the pharmacologic blockade of central muscarinic receptors in the aged that results in the selective disruption of verbal recall in secondary memory.

Aged↗