Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153640 (Cerebellum)
 1,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Separate murine knockout (KO) of either c- or N-myc genes in neural stem and precursor cells (NSC) driven by nestin-cre causes microcephaly. The cerebellum is particularly affected in the N-myc KO, leading to a strong reduction in cerebellar granule neural progenitors (CGNP) and mature granule neurons. In humans, mutation of N-myc also causes microcephaly in Feingold Syndrome. We created a double KO (DKO) of c- and N-myc using nestin-cre, which strongly impairs brain growth, particularly that of the cerebellum. Granule neurons were almost absent from the Myc DKO cerebellum, and other cell types were relatively overrepresented, including astroglia, oligodendrocytes, and Purkinje neurons. These findings are indicative of a profound disruption of cell fate of cerebellar stem and precursors. DKO Purkinje neurons were strikingly lacking in normal arborization. Inhibitory neurons were ectopic and exhibited very abnormal GAD67 staining patterns. Also consistent with altered cell fate, the adult DKO cerebellum still retained a residual external germinal layer (EGL). CGNP in the DKO EGL were almost uniformly NeuN and p27KIP1 positive as well as negative for Math1 and BrdU at the peak of normal cerebellar proliferation at P6. The presence of some mitotic CGNP in the absence of S phase cells suggests a possible arrest in M phase. CGNP and NSC metabolism also was affected by loss of Myc as DKO cells exhibited weak nucleolin staining. Together these findings indicate that c- and N-Myc direct cerebellar development by maintaining CGNP and NSC populations through inhibiting differentiation as well as directing rapid cell cycling and active cellular metabolism.
Cerebellum 2010 Dec
PMID:c- and N-myc regulate neural precursor cell fate, cell cycle, and metabolism to direct cerebellar development. 2065 25

Parkinson disease is the second most common neurodegenerative disease affecting elderly patients. It occurs due to the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). We continue our work in this model focusing on other brain areas affected with this disorder; cerebral cortex and cerebellum (areas other than substantia nigra) for better understanding the motor and behavior effect of the Parkinson disease as a forward steep for its treatment and medical control. This work aims to evaluate the therapeutic effect of stem cell-conditioned medium in the Parkinsonism model. In this study, Parkinsonism model was induced in rats by daily subcutaneous injection of 0.5 mg/Kg of rotenone for 28 days. Thirty rats were divided randomly into 3 groups; control, Parkinson, and conditioned medium (CM) treated groups. Cerebral Cortex and Cerebellum were obtained for histological, immunohistochemical and biochemical studies. In the Parkinsonism group, marked histological changes were observed. These findings were nearly ameliorated in CM treated group as confirmed by the biochemical, histological, and immunohistochemical (anti-alpha synculein, anti GFAP and anti nestin) studies. It could be concluded that CM had a good therapeutic effect on Parkinsonism induced damage in both the cerebral cortex and cerebellum.
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PMID:Cerebral and cerebellar histological changes in the rat animal model of rotenone induced parkinsonism can be ameliorated by bone marrow derived stem cell conditioned media. 3322 Apr 28