TMEM16F regulates pathologic α-synuclein secretion and spread in cellular and mouse models of Parkinson's disease.

One of the main hallmarks of Parkinson's disease (PD) pathology is the spread of the aggregate-prone protein α-synuclein (α-syn), which can be detected in the plasma and cerebrospinal fluid of patients as well as in the extracellular environment of neuronal cells. The secreted α-syn can exhibit "prion-like" behavior and transmission to naïve cells can promote conformational changes and pathology. The precise role of plasma membrane proteins in the pathologic process of α-syn is yet to be fully resolved.

Device for detection of activity-dependent changes in neural spheroids at MHz and GHz frequencies.

Intracellular processes triggered by neural activity include changes in ionic concentrations, protein release, and synaptic vesicle cycling. These processes play significant roles in neurological disorders. The beneficial effects of brain stimulation may also be mediated through intracellular changes.

Sympathetic response following unannounced loss of balance during walking in young adults: laboratory study.

An unannounced balance loss during walking, i.e., balance perturbation, is a stressful event, which changes the activity of the sympathetic nervous system (SNS).

Characteristics of Unsuccessful Balance Reactive Responses to Lateral Loss of Balance in Older Adults.

Introduction: An effective reactive step response to an unexpected balance loss is an important factor that determines if a fall will happen. We investigated reactive step strategies and kinematics of unsuccessful balance recovery responses that ended with falls in older adults.

Methods: We compared the strategies and kinematics of reactive stepping after a lateral loss of balance, i.

Disease-associated polyalanine expansion mutations impair UBA6-dependent ubiquitination.

Expansion mutations in polyalanine stretches are associated with a growing number of diseases sharing a high degree of genotypic and phenotypic commonality. These similarities prompted us to query the normal function of physiological polyalanine stretches and to investigate whether a common molecular mechanism is involved in these diseases. Here, we show that UBA6, an E1 ubiquitin-activating enzyme, recognizes a polyalanine stretch within its cognate E2 ubiquitin-conjugating enzyme USE1.