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Recent large-scale genome-wide studies for many human disorders have identified associations with numerous genetic variants. The biological interpretation of these variants presents a major challenge. In particular, the identification of biological pathways underlying the association could provide crucial insights into the disease aetiologies. In this thesis, I used functional genomics approaches to increase our understanding of neuropsychiatric and neurodevelopmental disorders. Firstly, in an integrative analysis of autism spectrum disorder (ASD), I looked into the role of genes targeted by Fragile-X Mental Retardation Protein ("FMRP targets"). I found evidence that FMRP targets contribute to ASD via two distinct aetiologies: (1) ultra-rare and highly penetrant single disruptions of embryonically upregulated FMRP targets ("single-hit aetiology") or (2) the combination of multiple less penetrant disruptions of synaptic FMRP targets ("multiple-hit aetiology"). In particular, I developed a pathway-association test sensitive to multiple-hit aetiologies. Secondly, I carried out an integrative analysis of bipolar disorder, following up a previously identified association with long-term potentiation. The association was not consistent across independent SNP and CNV datasets. Thirdly, I addressed the difficulty in identifying functional relationships between genes by integrating different datasets into a gene functional-linkage network tuned to the nervous system ("NsNet"). NsNet identified functional links between the genes disrupted by de novo loss-of-function mutations in ASD and, separately, in schizophrenia probands more sensitively than a general functional-linkage network. Fourthly, I considered the challenge of interpreting the phenotypic impact of gene disruptions, focusing on the identification of haploinsufficient genes. I constructed a gene haploinsufficiency score based on genome-wide datasets. Compared to existing approaches, the new score performed better in identifying less-studied haploinsufficient genes. This work both extends the methodology to detect the contribution of genetic variation to neuropsychiatric disorders and also yields insights into the variant genes and the pathways that underlie them. Firstly, in an integrative analysis of autism spectrum disorder (ASD), I looked into the role of genes targeted by Fragile-X Mental Retardation Protein ("FMRP targets"). I found evidence that FMRP targets contribute to ASD via two distinct aetiologies: (1) ultra-rare and highly penetrant single disruptions of embryonically upregulated FMRP targets ("single-hit aetiology") or (2) the combination of multiple less penetrant disruptions of synaptic FMRP targets ("multiple-hit aetiology"). In particular, I developed a pathway-association test sensitive to multiple-hit aetiologies. Secondly, I carried out an integrative analysis of bipolar disorder, following up a previously identified association with long-term potentiation. The association was not consistent across independent SNP and CNV datasets. Thirdly, I addressed the difficulty in identifying functional relationships between genes by integrating different datasets into a gene functional-linkage network tuned to the nervous system ("NsNet"). NsNet identified functional links between the genes disrupted by de novo loss-of-function mutations in ASD and, separately, in schizophrenia probands more sensitively than a general functional-linkage network. Fourthly, I considered the challenge of interpreting the phenotypic impact of gene disruptions, focusing on the identification of haploinsufficient genes. I constructed a gene haploinsufficiency score based on genome-wide datasets. Compared to existing approaches, the new score performed better in identifying less-studied haploinsufficient genes. This work both extends the methodology to detect the contribution of genetic variation to neuropsychiatric disorders and also yields insights into the variant genes and the pathways that underlie them.

Quantum phase transitions occur strictly at zero temperature and are accessed by varying a physical parameter such as a magnetic field or chemical potential. While these transitions themselves are experimentally inaccessible, the existence of a zero temperature quantum critical point has remarkable effects on the dynamical properties of interacting quantum many-body systems at finite temperatures. In this thesis, we study dynamics in four strongly interacting many-body systems near quantum critical points in the context of NMR relaxation, quantum quenches, many-body quantum chaos, and charge diffusion. In chapter 1, we begin by revisiting the issue of NMR relaxation in the quantum disordered phase of Ising spin chains. We find that the imaginary part of the spin susceptibility at low frequences is dominated by rare quantum processes which leads to an NMR relaxation rate that scales as $1/T_{1}\sim \exp(-\frac{2\Delta}{T})$ near the quantum critical point rather than the previously conjectured $1/T_{1}\sim \exp(-\frac{\Delta}{T})$. These results resolve certain discrepancies between the energy scales measured with different experimental probes in the quantum disordered paramagnetic phase of the Ising chain system $\text{CoNb}_{2}\text{O}_{6}$. In chapter 2, we study the non-equilibrium dynamics of Sachdev-Ye-Kitaev (SYK) models with $q$ body interactions after a quantum quench, considering a quench protocol which drives the system from an initial state with long-lived quasiparticle excitations to a final state lacking any long-lived quasiparticle excitations. For $q=4$, we find that the timescale for the system to locally thermalize $\tau_{eq}\sim\frac{\hbar}{k_{B}T}$ and for $q\rightarrow \infty$ we find that the system thermalizes instantaneously. In chapter 3, we study the real time dynamics of quantum electrodynamics in 2+1 dimensions with $N_{f}$ flavors of fermions. We focus on thermalization and the onset of many-body quantum chaos and compute the quantum Lyapunov exponent in a $\frac{1}{N_{f}}$ expansion. We briefly comment on chaos, locality, and gauge invariance. Finally, in Chapter 4 we consider whether the butterfly velocity - a speed at which quantum information propagates - may provide a fundamental bound on diffusion constants in dirty incoherent metals by computing the charge diffusion constant and the butterfly velocity in charge-neutral holographic matter with long wavelength ``hydrodynamic" disorder. In this limit, we find that the butterfly velocity does not set a sharp lower bound for the charge diffusion constant.