Prenatal protein malnutrition in rats alters the c-Fos response of neurons in the anterior cingulate and medial prefrontal region to behavioral stress.

Prenatal protein malnutrition affects brain development and behavior despite dietary rehabilitation from birth. Behavioral alterations include abnormal responses to stressors. To explore what brain regions mediate this altered response, we used immunocytochemistry to c-Fos protein, a transcription factor marking neuronal activation.

Melatonin promotes sleep in three species of diurnal nonhuman primates.

Nocturnal melatonin secretion is concurrent with consolidated sleep episodes in diurnal mammals and physiological melatonin levels can promote sleep onset in humans and in pigtail macaques. In order to further investigate the effects of melatonin treatment on sleep parameters in diurnal nonhuman primates, three macaque species have been studied: Macaca nemestrina, Macaca fascicularis, and Macaca mulatta. Sleep was assessed using continuous actigraphic recording of motor activity in animals maintained under 12:12-h light/dark cycle.

Elevated levels of the endosomal-lysosomal proteinase cathepsin D in cerebrospinal fluid in Alzheimer disease.

Lysosomal hydrolases are normally intracellular enzymes but are abundant extracellularly within senile plaques in Alzheimer disease and in other conditions where beta-amyloid accumulates. To examine whether acid hydrolases released from abnormal hydrolase-laden neurons are detectable in CSF, we measured levels of the major aspartic proteinase of lysosomes, cathepsin D (Cat D), in ventricular CSF collected after death from 30 patients with Alzheimer disease, 14 patients with Huntington disease, and seven patients with other neurodegenerative diseases. The levels of Cat D-immunoreactive protein, expressed as micrograms per milliliter of protein, determined by western blot immunoassay using a polyclonal antiserum against human brain Cat D, were more than fourfold higher in the Alzheimer patients than in the other patient groups (p < 0.

Diffuse Lewy body disease: light and electron microscopic immunocytochemistry of senile plaques.

The nature of senile plaques (SP) in 27 cases of diffuse Lewy body disease (LBD) was investigated using immunocytochemistry and antibodies to beta amyloid protein synthetic peptides (BetaSP), ubiquitin (UBQ), paired helical filaments (PHF; Ab39) and a 68-kDa protein in Alzheimer brains (Alz50). Lewy bodies were present in widespread areas of the neocortex of all cases and were more easily detected with ubiquitin immunocytochemistry than with conventional stains. All cases had neocortical SP, but only six cases had neocortical neurofibrillary tangles (NFT).