Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nerve growth factor (NGF) is a polypeptide that is necessary for the survival and growth of developing sympathetic and sensory neurons as well as basal forebrain cholinergic neurons in the brain. The effects of NGF are mediated by the binding of the factor to its specific receptor present on the surface of NGF-responsive cells. Since NGF-responsive basal forebrain cholinergic neurons are lost in Alzheimer's disease, treatment with NGF may be therapeutically beneficial for the patients with this disease. Our studies were focused on the purification, amino acid sequence, enzyme immunoassay (EIA), NGF-biosynthesizing cells, regulation of the biosynthesis, compounds stimulating NGF-biosynthesis/secretion, etc. The major results obtained are summarized as follows: 1) We purified NGFs from snake venoms and determined their amino acid sequences. Among them, Crotalus adamanteus-and Vipera russelli-NGFs were glycoproteins. 2) We developed highly sensitive (0.03-0.05 pg/tube or bead), simple, and reliable EIA systems for NGFs and NT-3. 3) Catecholamine, its derivatives, p-quinone derivatives, nicotine, nicotine derivatives, coenzymes, etc. enhanced the NGF-biosynthesis/secretion of fibroblasts and astrocytes by increasing their cellular content of NGF mRNA. 4) Basal forebrain-lesioned rats (an animal model of amnesia) administered 6-(4-hydroxybutyl)-2,3,5-trimethyl-1,4-benzoquinone (TMQ) orally showed improvement not only their NGF level and choline acetyltransferase (CAT) activity in the brain but also their memory and learning. 5) Interleukins (IL)-4 and -5 significantly increased the amounts of NGF secreted by mouse astrocytes; whereas IL-2, -3, and -6 had no significant effect. 6) Interferons-beta and -lambda inhibited the DNA- and NGF-synthesis in growing astrocytes cultured from neonatal mouse brain but they had no effect on the NGF-synthesis/secretion in quiescent astrocytes. 7) Alkylcatechols regulated the NGF gene expression in astrocytes via both protein kinase C- and cAMP-independent mechanisms.
 ...
PMID:[Biochemical studies on functional proteins in the brain nervous system. Neurobiochemical studies on nerve growth factor]. 870 5

A bidirectional flow of informations exists between the central nervous system and the immune system. Cytokines play a crucial role in this communication and exert several neuromodulatory actions. This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice. We interpret these behavioral and biochemical observations to indicate that the cytokine-to-brain communication can result in alterations in brain functions.
 ...
PMID:Cytokines and cognitive function in mice 958 25

A bidirectional flow of informations exists between the central nervous system and the immune system. Cytokines play a crucial role in this communication and exert several neuromodulatory actions. This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice. We interpret these behavioral and biochemical observations to indicate that the cytokine-to-brain communication can result in alterations in brain functions.
 ...
PMID:Cytokines and cognitive function in mice. 964 97

Loss of memory B cells occurs from the onset of HIV-1 infection and persists into the chronic stages of infection. Lack of survival of these cells, even in subjects being treated, could primarily be the consequence of an altered local microenvironment induced by HIV infection. In this study we showed that memory B cell survival was significantly decreased in aviremic successfully treated (ST) subjects compared with subjects who control viral load as a result of natural immunity (elite controller [EC]) or with uninfected control (HIV-) subjects. The lower survival levels observed in memory B cells from ST subjects were the result of disrupted IL-2 signaling that led to increased transcriptional activity of Foxo3a and increased expression of its proapoptotic target TRAIL. Notably, memory B cell survival in ST subjects was significantly enhanced by the addition of exogenous IL-2 in a Foxo3a-dependent manner. We further showed that Foxo3a silencing by siRNA resulted in decreased expression of TRAIL and apoptosis levels in memory B cells from ST subjects. Our results thus establish a direct role for Foxo3a/TRAIL signaling in the persistence of memory B cells and provide a mechanism for the reduced survival of memory B cells during HIV infection. This knowledge could be exploited for the development of therapeutic and preventative HIV vaccines.
 ...
PMID:Loss of memory B cells during chronic HIV infection is driven by Foxo3a- and TRAIL-mediated apoptosis. 2192 63