Disease relevance of Psen2

• Presenilins in the heart: presenilin-2 expression is increased by low glucose and by hypoxia in cardiac cells [1].

Psychiatry related information on Psen2

• Presenilin-2 has previously been associated with intercellular signaling in the central nervous system, in Alzheimer's disease [1].

High impact information on Psen2

• The presenilin-2 loop peptide perturbs intracellular Ca2+ homeostasis and accelerates apoptosis [2].
• Previous studies have demonstrated the molecular linkage of three causative genes for early-onset Alzheimer's disease: the presenilin 1 gene on chromosome 14, the presenilin 2 gene on chromosome 1, and the amyloid precursor protein gene on chromosome 21 [3].
• PS-1 and PS-2 transcripts were reduced in hippocampus and neocortex [4].
• Glucose deprivation itself caused significant up-regulation of the presenilin-2 (to 160%) and with low oxygen increased presenilin-2 level to over 200% of the control [1].
• The finding of presenilin-2 in the heart and the responsiveness to low glucose and hypoxia suggests that PS2 may be regulated by conditions of ischemia, a condition which both the heart and brain may experience [1].

Biological context of Psen2

• RESULTS: IK was increased in cultured rat hippocampal neurons, after transient transfection of PS-1, PS-2, and APP695 [5].

Anatomical context of Psen2

• In BHK fibroblasts, both PS1 and PS2 independently inhibit somatostatin gene in non-islet cells [6].
• In this study, exposing PC12 cells expressing mutant presenilin 2 to 50 microM AP25-35, 30 mM L-glutamate and 50 microM H2O2 caused a significant increase in acetylcholine esterase activity [7].

Associations of Psen2 with chemical compounds

• PS2 was much more inhibited during propofol-induced sleep, than during the pretreatment period, consistent with an expected marked increase in recurrent inhibition [8].
• Sevoflurane 2.0 vol% significantly enhanced paired-pulse (PS2/PS1) facilitation (from 128.4% to 155.5% at an inter-stimulus interval of 37.9 ms); this enhancement was blocked by phaclofen [9].
• At higher stimulation intensities, however, baclofen (30 mg/kg iv) increased PS2, while barely affecting the population spike in BIC-treated animals [10].

Regulatory relationships of Psen2

• These results suggest that a mutant presenilin 2-induced neurodegeneration in Alzheimer's disease might be involved in the increase in acetylcholinesterase activity [7].

Analytical, diagnostic and therapeutic context of Psen2

• RT-PCR confirmed the presence of PS2 in the heart of adult rats.Using quantitative real-time RT-PCR, we further studied the expression of presenilin-2 mRNA under conditions of low oxygen supply and glucose starvation [1].

References