Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C1519176 (
PSA
)
5,490
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Neonatal hypoxia-ischemia (nHI) disrupts hippocampal GABAergic development leading to memory deficits in mice. Polysialic-acid neural-cell adhesion molecule (PSA-NCAM) developmentally declines to trigger GABAergic maturation. We hypothesized that nHI changes
PSA
-NCAM abundance and cellular distribution, impairing GABAergic development, and marking nascent neurodegeneration. Cell degeneration, atrophy, and
PSA
-NCAM immunoreactivity (IR) were measured in CA1 of nHI-injured C57BL6 mice related to: (i) cellular subtype markers; (ii) GAD65/67 and synatophysin (SYP), pre-synaptic markers; (iii) phospho-Ser
396
Tau, cytoskeletal marker; and (iv)
GAP43
, axonalregeneration marker.
PSA
-NCAM IR was minimal in CA1 of shams at P11. After nHI,
PSA
-NCAM IR was increased in injured pyramidal cells (PCs), minimal in parvalbumin (PV)
+
INs, and absent in glia.
PSA
-NCAM IR correlated with injury severity and became prominent in perikaryal cytoplasm at P18. GAD65/67 and SYP IRs only weakly related to
PSA
-NCAM after nHI. Injured phospho-Ser
396
Tau
+
PCs and PV
+
INs variably co-expressed
PSA
-NCAM at P40. While PCs with cytoplasmic marginalized
PSA
-NCAM had increased perisomatic
GAP43
, those with perikaryal cytoplasmic
PSA
-NCAM had minimal
GAP43
.
PSA
-NCAM increased in serum of nHI-injured mice. Increased
PSA
-NCAM is likely a generic acute response to nHI brain injury.
PSA
-NCAM aberrant cellular localization may aggravate neuronal degeneration. The significance of
PSA
-NCAM as a biomarker of recovery from nHI and nascent neurodegeneration needs further study.
...
PMID:Accumulation of PSA-NCAM marks nascent neurodegeneration in the dorsal hippocampus after neonatal hypoxic-ischemic brain injury in mice. 3270 9
