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We are performing additional analyses to determine potential impact of these findings in AD. We will also perform rare variant, gene-based, and additional pathway analyses.
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Suicide is a serious public health problem, resulting in the loss of hundreds of thousands of lives each year and contributing to pain, sorrow, and loss in affected friends, families, and communities. There is compelling evidence that suicide aggregates in families, that genes account for some of the observed variability in suicidal behavior, and that its genetic transmission is potentially distinct from that of psychiatric disorders.
In light of this understanding, researchers have channeled their efforts toward determining the molecular genetic basis for suicide. Unfortunately, molecular analyses have yielded highly inconsistent findings, and their collective interpretation does not allow definitive conclusions about the contributions of specific genes to the pathophysiology of suicide.
One reason for the inconsistency of previous findings may be the heterogeneity of suicide phenotypes. The present study attempts to replicate previous genetic associations in the context of a more narrowly defined sample of suicide decedents with personality disorder PD diagnoses.
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Suicidality and PDs frequently co-occur and many outcomes associated with personality pathology e. Moreover, given that PDs, and personality traits more broadly, appear to be heritable, suicide in the context of PDs may have a substantial genetic component. Samples from 85 Utah suicide decedents with a history of a personality disorder PD diagnosis were included in analyses.
This produced a subset of 83 genes with 1, total loci for analyses in the Exome Chip sample, and 84 genes with 4, loci in the PsychArray sample.
Chi-square analyses were used to indicate variants that were over-represented in decedents with personality pathology compared to a population of publically available control subjects of Northern European descent. Additionally, diagnostic and demographic information from the sample was compared to a larger database of 9, recorded suicide cases in Utah. Results: Compared to other Utah suicides, the sample of PD decedents was younger and more likely to be female.
PD decedents also had higher rates of all analyzed psychiatric and medical diagnoses. Although previous research has linked variation on ANO5 with suicide, DDC may represent the best candidate for further research. The ANO5 gene codes for the protein anoctamin-5, which is found in the skeletal and cardiac muscles and in bone cells.
However, the specific function of ANO5 is not well understood. Alternatively, DDC is known to catalyze the biosynthesis of neurotransmitters dopamine and serotonin, and in tryptamine, which acts as a non-selective serotonin receptor agonist. Additionally, COMT—which also contained significant variation in our sample— is also implicated in the dopaminergic synaptic pathway. Acute amphetamine administration increases locomotion and enhances activation of D1-expressing medium spiny neurons in the mouse dorsal striatum.
Amphetamine also has a high potential for abuse and addiction. There is much evidence supporting the role of the nucleus accumbens ventral striatum in addiction-like behaviors. These neurons project to the substantia nigra pars reticulata and the internal segment of the globus pallidus termed the direct pathway.
We then implanted imaging fibers into the same location and recorded calcium transients in mice treated with acute amphetamine or saline in their home cage. We found that amphetamine produced and enhancement of locomotion that correlated with increases in calcium transients in the D1MSNs suggesting that amphetamine may modulate the direct path in the dorsal striatum. Gene expression profiling reveals altered neurodevelopmental transcriptional networks in heterozygous Chd8 mice.
The high-confidence autism risk gene CHD8, a chromatin remodeling factor, has emerged as a potential master regulator of pathways implicated in autism and neurodevelopmental disorders. We performed RNA-sequencing on forebrain of heterozygous and wild-type mice across development at embryonic days e Down-regulated genes are most strongly enriched in RNA processing networks and regulation of gene expression.
Co-expression network analysis identified networks implicated in other autism genetic studies, as well as perturbed networks that result in a shift toward increased proliferation in early brain development. Our results suggest that haploinsufficiency of Chd8 disrupts the developmental cell state and highlight the convergence of chromatin remodeling, RNA processing, and neuronal differentiation as principle gene networks potentially involved in the genetic and neurodevelopmental origins of autism spectrum disorders.
Epilepsy in females with mental retardation EFMR is an infantile epileptic disease often accompanying intellectual disabilities, which has rare inheritance patterns. Unlike the typical X-linked mode of inheritance, in which males are affected and females are unaffected carriers, EFMR only seems to affect heterozygous females and not males. The biochemical and developmental properties of PCDH19 and its function in neurons are currently unknown, making it difficult to establish the pathophysiological mechanism of EFMR.
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We checked the developmental profile of PCDH19 at different developmental time points in different regions of the brain. The expression level gradually increases until post-natal day 7 P7 and it dramatically decreases after this particular time point, but not their mRNA transcript levels.
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By treating several secretase inhibitors on both in-vitro and in-vivo models, we found that just like other membrane embedded proteins, PCDH19 also undergo secretase-dependent cleavage process and the fragmented C-terminus translocate to the nucleus. Moreover, we checked through if this secretase dependent cleavage is also time-dependent using immunostaining.
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The C-terminus of PCDH19 is located outside the nucleus during the early developmental period, but it is located within the nucleus as neurons mature in rat primary cultured neurons. Moreover, PCDH19 is enriched in the exons and dendrites in the immature primary cultured neurons, promoting the synapse formation in the artificial synapse formation assay, but it gradually decreases from axons as neurons develop.
Taken together, PCDH19 is a neural adhesion molecule that has homophilic interaction, and its biochemical properties are highly time-dependent, suggesting cell-cell interaction during brain development is the biological process that could be relevant to the pathophysiology of EFMR. Bipolar Disorder BD is a psychiatric illness characterized by mood disturbances and abnormal circadian rhythms. Lithium restores circadian rhythms in sleep and activity, in part through its effects on PER2 expression.
By inhibiting inositol monophosphatases IMPs , lithium alters inositol metabolism. However, the precise means by which lithium acts upon the circadian clock genes like PER2 are not yet fully established. IMP inhibition by lithium extends the duration of IP3, and its conversion to higher order inositol polyphosphates. In an effort to identify new pathways for mood stabilizer development in BD, we examined whether inositol pathways engaged by lithium have effects on circadian rhythms in cells.
We used mouse NIH3T3 cells transfected with Perluc, a circadian bioluminescent reporter to study rhythms for days under constant conditions. We examined whether higher order metabolites of myo-inositol like inositol hexaphosphate IP6 have effects on circadian rhythms in cells that resemble the effect of lithium. Treatment of cells with APB, an IP3R antagonist shortened period, reversed the period lengthening effects of lithium, but had no effect on amplitude.
Accordingly, IP6 increased rhythm amplitude and shortened period. IP6 is converted by IP6Ks into inositol pyrophosphates. IP3 affects period. IP6 affects amplitude, and may involve inhibition of GSK3B through an inositol pyrophosphate mechanism as a critical step.
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Inositol phosphates may offer a novel means through which circadian rhythms can be regulated. Identifying suicide genetic risk variants in a high-risk pedigree with a significant increase of female suicides. Suicide is a significant health issue, accounting for over , deaths per year globally. Moreover, there is a significant gender difference in suicide completion.