Superior High Transistor's Effective Mobility of 325 cm2/V-s by 5 nm Quasi-Two-Dimensional SnON nFET.

This work reports the first nanocrystalline SnON (7.6% nitrogen content) nanosheet n-type Field-Effect Transistor (nFET) with the transistor's effective mobility (µeff) as high as 357 and 325 cm2/V-s at electron density (Qe) of 5 × 1012 cm-2 and an ultra-thin body thickness (Tbody) of 7 nm and 5 nm, respectively. At the same Tbody and Qe, these µeff values are significantly higher than those of single-crystalline Si, InGaAs, thin-body Si-on-Insulator (SOI), two-dimensional (2D) MoS2 and WS2. The new discovery of a slower µeff decay rate at high Qe than that of the SiO2/bulk-Si universal curve was found, owing to a one order of magnitude lower effective field (Eeff) by more than 10 times higher dielectric constant (κ) in the channel material, which keeps the electron wave-function away from the gate-oxide/semiconductor interface and lowers the gate-oxide surface scattering. In addition, the high µeff is also due to the overlapped large radius s-orbitals, low 0.29 mo effective mass (me*) and low polar optical phonon scattering. SnON nFETs with record-breaking µeff and quasi-2D thickness enable a potential monolithic three-dimensional (3D) integrated circuit (IC) and embedded memory for 3D biological brain-mimicking structures.

A biomarker-authenticated model of schizophrenia implicating NPTX2 loss of function.

Schizophrenia is a polygenetic disorder whose clinical onset is often associated with behavioral stress. Here, we present a model of disease pathogenesis that builds on our observation that the synaptic immediate early gene NPTX2 is reduced in cerebrospinal fluid of individuals with recent onset schizophrenia. NPTX2 plays an essential role in maintaining excitatory homeostasis by adaptively enhancing circuit inhibition. NPTX2 function requires activity-dependent exocytosis and dynamic shedding at synapses and is coupled to circadian behavior. Behavior-linked NPTX2 trafficking is abolished by mutations that disrupt select activity-dependent plasticity mechanisms of excitatory neurons. Modeling NPTX2 loss of function results in failure of parvalbumin interneurons in their adaptive contribution to behavioral stress, and animals exhibit multiple neuropsychiatric domains. Because the genetics of schizophrenia encompasses diverse proteins that contribute to excitatory synapse plasticity, the identified vulnerability of NPTX2 function can provide a framework for assessing the impact of genetics and the intersection with stress.

NPTX2 and cognitive dysfunction in Alzheimer's Disease.

Memory loss in Alzheimer's disease (AD) is attributed to pervasive weakening and loss of synapses. Here, we present findings supporting a special role for excitatory synapses connecting pyramidal neurons of the hippocampus and cortex with fast-spiking parvalbumin (PV) interneurons that control network excitability and rhythmicity. Excitatory synapses on PV interneurons are dependent on the AMPA receptor subunit GluA4, which is regulated by presynaptic expression of the synaptogenic immediate early gene NPTX2 by pyramidal neurons. In a mouse model of AD amyloidosis, Nptx2-/- results in reduced GluA4 expression, disrupted rhythmicity, and increased pyramidal neuron excitability. Postmortem human AD cortex shows profound reductions of NPTX2 and coordinate reductions of GluA4. NPTX2 in human CSF is reduced in subjects with AD and shows robust correlations with cognitive performance and hippocampal volume. These findings implicate failure of adaptive control of pyramidal neuron-PV circuits as a pathophysiological mechanism contributing to cognitive failure in AD.