Neuromorphic Learning towards Nano Second Precision

Temporal coding is one approach to representing information in spiking neural networks. An example of its application is the location of sounds by barn owls that requires especially precise temporal coding. Dependent upon the azimuthal angle, the arrival times of sound signals are shifted between both ears. In order to deter- mine these interaural time differences, the phase difference of the signals is measured. We implemented this biologically inspired network on a neuromorphic hardware system and demonstrate spike-timing dependent plasticity on an analog, highly accelerated hardware substrate. Our neuromorphic implementation enables the resolution of time differences of less than 50 ns. On-chip Hebbian learning mechanisms select inputs from a pool of neurons which code for the same sound frequency. Hence, noise caused by different synaptic delays across these inputs is reduced. Furthermore, learning compensates for variations on neuronal and synaptic parameters caused by device mismatch intrinsic to the neuromorphic substrate.Comment: 7 pages, 7 figures, presented at IJCNN 2013 in Dallas, TX, USA. IJCNN 2013. Corrected version with updated STDP curves IJCNN 201

Open-Cavity in Closed-Cycle Cryostat as a Quantum Optics Platform

The introduction of an optical resonator can enable efficient and precise interaction between a photon and a solid-state emitter. It facilitates the study of strong light-matter interaction, polaritonic physics and presents a powerful interface for quantum communication and computing. A pivotal aspect in the progress of light-matter interaction with solid-state systems is the challenge of combining the requirements of cryogenic temperature and high mechanical stability against vibrations while maintaining sufficient degrees of freedom for in situ tunability. Here, we present a fiber-based open Fabry-Pérot cavity in a closed-cycle cryostat exhibiting ultrahigh mechanical stability while providing wide-range tunability in all three spatial directions. We characterize the setup and demonstrate the operation with the root-mean-square cavitylength fluctuation of less than 90 pm at temperature of 6.5 K and integration bandwidth of 100 kHz. Finally, we benchmark the cavity performance by demonstrating the strong-coupling formation of exciton polaritons in monolayer WSe2 with a cooperativity of 1.6. This set of results manifests the open cavity in a closed-cycle cryostat as a versatile and powerful platform for low-temperature cavity QED experiments

Open-cavity in closed-cycle cryostat as a quantum optics platform

The introduction of an optical resonator can enable efficient and precise interaction between a photon and a solid-state emitter. It facilitates the study of strong light-matter interaction, polaritonic physics and presents a powerful interface for quantum communication and computing. A pivotal aspect in the progress of light-matter interaction with solid-state systems is the challenge of combining the requirements of cryogenic temperature and high mechanical stability against vibrations while maintaining sufficient degrees of freedom for in-situ tunability. Here, we present a fiber-based open Fabry-P\'{e}rot cavity in a closed-cycle cryostat exhibiting ultra-high mechanical stability while providing wide-range tunability in all three spatial directions. We characterize the setup and demonstrate the operation with the root-mean-square cavity length fluctuation of less than $90$ pm at temperature of $6.5$ K and integration bandwidth of $100$ kHz. Finally, we benchmark the cavity performance by demonstrating the strong-coupling formation of exciton-polaritons in monolayer WSe$_2$ with a cooperativity of $1.6$. This set of results manifests the open-cavity in a closed-cycle cryostat as a versatile and powerful platform for low-temperature cavity QED experiments.Comment: 10 pages, 8 figure

Biomarker candidates of neurodegeneration in Parkinson’s disease for the evaluation of disease-modifying therapeutics

Reliable biomarkers that can be used for early diagnosis and tracking disease progression are the cornerstone of the development of disease-modifying treatments for Parkinson’s disease (PD). The German Society of Experimental and Clinical Neurotherapeutics (GESENT) has convened a Working Group to review the current status of proposed biomarkers of neurodegeneration according to the following criteria and to develop a consensus statement on biomarker candidates for evaluation of disease-modifying therapeutics in PD. The criteria proposed are that the biomarker should be linked to fundamental features of PD neuropathology and mechanisms underlying neurodegeneration in PD, should be correlated to disease progression assessed by clinical rating scales, should monitor the actual disease status, should be pre-clinically validated, and confirmed by at least two independent studies conducted by qualified investigators with the results published in peer-reviewed journals. To date, available data have not yet revealed one reliable biomarker to detect early neurodegeneration in PD and to detect and monitor effects of drug candidates on the disease process, but some promising biomarker candidates, such as antibodies against neuromelanin, pathological forms of α-synuclein, DJ-1, and patterns of gene expression, metabolomic and protein profiling exist. Almost all of the biomarker candidates were not investigated in relation to effects of treatment, validated in experimental models of PD and confirmed in independent studies

Genome sequencing analysis identifies new loci associated with Lewy body dementia and provides insights into its genetic architecture

The genetic basis of Lewy body dementia (LBD) is not well understood. Here, we performed whole-genome sequencing in large cohorts of LBD cases and neurologically healthy controls to study the genetic architecture of this understudied form of dementia, and to generate a resource for the scientific community. Genome-wide association analysis identified five independent risk loci, whereas genome-wide gene-aggregation tests implicated mutations in the gene GBA. Genetic risk scores demonstrate that LBD shares risk profiles and pathways with Alzheimer's disease and Parkinson's disease, providing a deeper molecular understanding of the complex genetic architecture of this age-related neurodegenerative condition

Genome-wide structural variant analysis identifies risk loci for non-Alzheimer’s dementias

We characterized the role of structural variants, a largely unexplored type of genetic variation, in two non-Alzheimer’s dementias, namely Lewy body dementia (LBD) and frontotemporal dementia (FTD)/amyotrophic lateral sclerosis (ALS). To do this, we applied an advanced structural variant calling pipeline (GATK-SV) to short-read whole-genome sequence data from 5,213 European-ancestry cases and 4,132 controls. We discovered, replicated, and validated a deletion in TPCN1 as a novel risk locus for LBD and detected the known structural variants at the C9orf72 and MAPT loci as associated with FTD/ALS. We also identified rare pathogenic structural variants in both LBD and FTD/ALS. Finally, we assembled a catalog of structural variants that can be mined for new insights into the pathogenesis of these understudied forms of dementia

Mitochondrial haplogroups and cognitive progression in Parkinson's disease

International audienceMitochondria are a culprit in the onset of Parkinson's disease, but their role during disease progression is unclear. Here we used Cox proportional hazards models to exam the effect of variation in the mitochondrial genome on longitudinal cognitive and motor progression over time in 4064 patients with Parkinson's disease. Mitochondrial macro-haplogroup was associated with reduced risk of cognitive disease progression in the discovery and replication population. In the combined analysis, patients with the super macro-haplogroup J, T, U# had a 41% lower risk of cognitive progression with P = 2.42 × 10-6 compared to those with macro-haplogroup H. Exploratory analysis indicated that the common mitochondrial DNA variant, m.2706A>G, was associated with slower cognitive decline with a hazard ratio of 0.68 (95% confidence interval 0.56-0.81) and P = 2.46 × 10-5. Mitochondrial haplogroups were not appreciably linked to motor progression. This initial genetic survival study of the mitochondrial genome suggests that mitochondrial haplogroups may be associated with the pace of cognitive progression in Parkinson's disease over time