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Tau accumulation is a prominent feature in a variety of neurodegenerative disorders and remarkable effort has been expended working out the biochemistry and cell biology of this cytoplasmic protein. Tau’s wayward properties may derive from germline mutations in the case of frontotemporal lobar degeneration (FTLD-MAPT) but may also be prompted by less understood cues-perhaps environmental or from molecular damage as a consequence of chronological aging-in the case of idiopathic tauopathies. Tau properties are undoubtedly affected by its covalent structure and in this respect tau protein is not only subject to changes in length produced by alternative splicing and endoproteolysis, but different types of posttranslational modifications that affect different amino acid residues. Another layer of complexity concerns alternate conformations-“conformers”-of the same covalent structures; in vivo conformers can encompass soluble oligomeric species, ramified fibrillar structures evident by light and electron microscopyresent even within intermediate disease stages, likely mitigates against one-size-fits-all therapeutic strategies and may require a suite of interventions. We consider the extent to which animal models of tauopathy can be reasonably enrolled in the campaign to produce such interventions and to slow the otherwise inexorable march of disease progression.Coronavirus Disease 2019 (COVID-19), caused by the Severe Acute Respiratory Syndrome coronavirus-2 (SARS-CoV-2), began in December 2019, in Wuhan, China and was promptly declared as a pandemic by the World Health Organization (WHO). As an acute respiratory disease, COVID-19 uses the angiotensin-converting enzyme 2 (ACE2) receptor, which is the same receptor used by its predecessor, SARS-CoV, to enter and spread through the respiratory tract. Common symptoms of COVID-19 include fever, cough, fatigue and in a small population of patients, SARS-CoV-2 can cause several neurological symptoms. find more Neurological malaise may include severe manifestations, such as acute cerebrovascular disease and meningitis/encephalitis. Although there is evidence showing that coronaviruses can invade the central nervous system (CNS), studies are needed to address the invasion of SARS-CoV-2 in the CNS and to decipher the underlying neurotropic mechanisms used by SARS-CoV-2. This review summarizes current reports on the neurological manifestations of COVID-19 and addresses potential routes used by SARS-CoV-2 to invade the CNS.Objective To further understand the mechanisms underlying epileptic network and the characteristics of individual specific network, we conducted a study on brain network by magnetoencephalography (MEG) focusing on patients with childhood absence epilepsy (CAE). Methods The network connectivity of 22 patients was investigated with MEG at the source level. Network connectivity of spikes and slow waves was computed with accumulated source imaging (ASI) and correlation analysis. Time-frequency analysis was used to characterize the network changes during the ictal-onset period of each patient and the potential factors. Results We found that spectral power increased at around 1 s and distributed at 2-4 Hz in all patients. Ictal spikes simultaneously showed elevation of network connectivity, predominantly excitatory connections, when generalized firing activity spread to the overall brain. High-frequency oscillations (HFOs) were prone to detect overexcited neuronal firing in certain focal areas. Conclusions Personal network changes during ictal onset had unique features in the time range and parallel seizure rhythm uniformly in every patient. There was an important time point for generalized discharges of the epileptic network. Ictal spiking activity played an important role in the epileptic network synchronicity of childhood absence epilepsy. Frequency oscillations provided references for locating abnormal changes in neuromagnetic signals.While neuroimaging and blood biomarker have been two of the most active areas of research in the neurotrauma community, these fields rarely intersect to delineate subconcussive brain injury. The aim of the study was to examine the association between diffusion MRI techniques [diffusion tensor imaging (DTI) and neurite orientation/dispersion density imaging (NODDI)] and brain-injury blood biomarker levels [tau, neurofilament-light (NfL), glial-fibrillary-acidic-protein (GFAP)] in high-school football players at their baseline, aiming to detect cumulative neuronal damage from prior seasons. Twenty-five football players were enrolled in the study. MRI measures and blood samples were obtained during preseason data collection. The whole-brain, tract-based spatial statistics was conducted for six diffusion metrics fractional anisotropy (FA), mean diffusivity (MD), axial/radial diffusivity (AD, RD), neurite density index (NDI), and orientation dispersion index (ODI). Five players were ineligible for MRIs, and three serum samples were excluded due to hemolysis, resulting in 17 completed set of diffusion metrics and blood biomarker levels for association analysis. Our permutation-based regression model revealed that serum tau levels were significantly associated with MD and NDI in various axonal tracts; specifically, elevated serum tau levels correlated to elevated MD (p = 0.0044) and reduced NDI (p = 0.016) in the corpus callosum and surrounding white matter tracts (e.g., longitudinal fasciculus). Additionally, there was a negative association between NfL and ODI in the focal area of the longitudinal fasciculus. Our data suggest that high school football players may develop axonal microstructural abnormality in the corpus callosum and surrounding white matter tracts, such as longitudinal fasciculus. A future study is warranted to determine the longitudinal multimodal relationship in response to repetitive exposure to sports-related head impacts.Background Essential tremor (ET) encompasses a variety of features, including tremor, cognitive dysfunction, and gait and balance impairments. Gait and balance impairments in ET are often mild, but they can be severe and are, in some cases, associated with functional sequelae in terms of increased fall risk and reduced balance confidence. Previous research on gait and balance in ET has been limited to cross-sectional comparisons. There have been no longitudinal studies or prospective studies. As such, our understanding of natural history and possible predictors of declines in ET-related gait and balance impairments is incomplete. Objectives We (1) present natural history data on the change in gait and balance measures over time, (2) provide estimates of annual rate of change in each gait and balance metric, and (3) examine the relationship between baseline clinical predictors and changes in gait and balance over time. Methods 149 ET participants (mean age 78.7 years), enrolled in a prospective, longitudinal, clinical-pathological study, underwent an extensive evaluation of cognition, tremor, and gait and balance at three distinct intervals performed every 18 months.