Provided herein are compositions comprising light-activated chimeric proteins expressed on plasma membranes and methods of using the same to selectively depolarize excitatory or inhibitory neurons.

The invention relates to mutant NQ-Rhodopsin having potassium pumping properties, nucleic acid constructs encoding same, expression vectors carrying the nucleic acid construct, cells comprising said nucleic acid construct or expression vector, and their respective uses.

Disclosed are methods of detecting abnormal expression of one or more genes associated with a neurological disease such as the Alexander disease, the Alzheimer's disease, the Parkinson disease, the Huntington disease, multiple sclerosis, and amyotrophic lateral sclerosis. The methods include performing a transcriptome analysis of the astrocytes derived from a patient and the astrocytes derived from a healthy control subject, thereby to determine one or more genes that are substantially differentially expressed. Also disclosed are methods of treating a neurological disease by correcting the abnormally expressed genes associated with the neurological disease.

Disclosed herein are devices including a substrate, one or more regions of electrically active material, and optionally at least one electrode. Also disclosed herein are devices or systems including a substrate, one or more regions of electrically active material including muscle cells and neuronal cells, and optionally at least one electrode. In some embodiments, the muscle cells and neuronal cells form one or more neuromuscular junctions at defined locations on the electrically active material. Also disclosed are methods of using the devices and systems for analyzing the effect of compounds on neuronal cell, muscle cell and/or neuromuscular junction activity.

Methods for treatment and diagnosis of neurological disorders such as autism and autism spectrum disorder are disclosed. Also disclosed are modulators of alternative splicing regulators SRRM4 and/or SRRM3 for treating neurological disorders. Further disclosed are agents that modulate the expression of at least one splice variant for treating neurological disorders. Mouse models of neurological disorders having increased or decreased expression of SRRM4 and/or SRRM3 are also disclosed.

The present subject matter provides a microfluidic device that enables the precise and repeatable three dimensional and compartmentalized coculture of muscle cells and neuronal cells. Related apparatus, systems, techniques, and articles are also described.

The present disclosure provides targeting peptides and vectors containing a sequence that encodes targeting peptides that deliver agents to the brain.

This invention relates to the use sigma-2 receptor antagonists, and of pharmaceutical compositions comprising such compounds, in methods for inhibiting Abeta-associated synapse loss or synaptic dysfunction in neuronal cells, modulating an Abeta-associated membrane trafficking change in neuronal cells, and treating cognitive decline associated with Abeta pathology and more broadly treating with such compounds and compositions neurodegenerative diseases and disorders associated with Abeta pathology. This invention also relates to methods for screening compounds for activity in inhibiting cognitive decline on the basis of their ability to bind to a sigma-2 receptor.

Aspects of the present disclosure include amyloid β (Aβ) peptides. In certain aspects, the Aβ peptides include a chiral substitution at an electrostatic cluster amino acid residue. Also provided are compositions, non-human animals, and kits that include the Aβ peptides. Methods involving the Aβ peptides are also provided.

Non-invasive method for diagnosing or prognosing Alzheimer's disease, frontotemporal dementia, or other dementia involving isolating astrocyte-derived exosomes (ADEs) and neuron-derived exosomes (NDEs) from a human biological sample (i.e., plasma, serum, urine or cerebrospinal fluid), analyzing cargo extracts of the ADEs and NDEs to detect at least one specified protein or microRNA biomarker, comparing the levels and activities of detected biomarker(s) to those in control samples to identify a statistically significant difference between the detected biomarker(s) and corresponding biomarker(s) in the control sample to determine presence of Alzheimer's disease, frontotemporal dementia, or other dementia; and testing effects of drugs on levels and activities of each biomarker, as well as effects of drugs administered to test subjects on levels and activities of each biomarker in ADEs and NDEs from subsequently obtained biological samples.