Brain-Decarboxylase Activities as Indices of Pathological Change in Senile Dementia

Vasopressin and Oxytocin Neurons of the Human Supraoptic and Paraventricular Nucleus; Size Changes in Relation to Age and Sex

“…asymmetry in the activity of AVP neurons may also be indirectly caused by the asymmetrical distribution of neurotransmitters in the human brain (64), such as ␥-aminobutyric acid (GABA), that is, in an opposite way from the activity of the AVP neurons, related to age and has right side prevalence in the brain (64). Indeed, the observation that GABA levels decrease with age in man (64,65) while it appears to have a striking inhibitory effect on AVP release in the PVN (66) and SON (67) make it an interesting potential factor involved in the age-and lateralization-related control of AVP neuronal activity. As the inhibitory effect of GABA decreases with aging (64,65), AVP neurons would become more active during the course of aging, as was indeed found earlier by the increased size of the Golgi apparatus (28,34) and in the present study for the cell size.…”

“…Indeed, the observation that GABA levels decrease with age in man (64,65) while it appears to have a striking inhibitory effect on AVP release in the PVN (66) and SON (67) make it an interesting potential factor involved in the age-and lateralization-related control of AVP neuronal activity. As the inhibitory effect of GABA decreases with aging (64,65), AVP neurons would become more active during the course of aging, as was indeed found earlier by the increased size of the Golgi apparatus (28,34) and in the present study for the cell size. It should be noted also that a lateralization of the SON would not have many functional implications, as it contains mainly neurosecretory neurons releasing their products into the bloodstream, whereas the PVN also has projections into the brain (1).…”

Increased response of serum prolactin to metoclopramide in senile dementia of Alzheimer type

“…(1979) found reduced postmortem levels of homovanillic acid (the main dopamine metabolite) in the caudate nucleus and other subcortical structures, and several studies have reported changes in the dopamine system in patients with SDAT (eg Gottfries et al, 1969;Bowen et al, 1974). However, in two studies levels of dopamine itself have been found to be no lower in SDAT than in age-matched controls (Yates et al, 1979, Mann et al, 1980 and in another study where there was a reduction in dopamine it was very restricted in distribution (Adolfsson et al, 1979).…”

Handbook of Psychopharmacology

“…Hagan pigmented cells from the locus ceruleus in the brains of Alzheimer's patients. His observations have been confirmed (Mann et at., 1980(Mann et at., , 1982, and depleted biochemical markers for norepinephrine, dopamine, and serotonin receptors (Adolfsson et Arai et at., 1984;Bowen et at., 1974;Crow et al, 1984;Mann et at., 1982;Tomlinson et at., 1981;Yates et at., 1983) have since been reported. Reductions in glutamate binding (Greenamyre et at., 1985), central nervous system (CNS) somatostatin levels (Davies et at., 1980;Serby et at., 1984), and an apparent vulnerability of somatostatin-containing cells (Roberts et at., 1985;Morrison et at., 1985) have also been reported.…”