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Pal, A.

Publications and source records attributed to Pal, A..

2 recordsLinked to original sources
bioRxiv2018

Neurobiological Basis of Brain Blood Oxygenation Responses Correlated with Cognitive Stroop Task Performance Before and After an Acute Bout of Aerobic Exercise

Cardiovascular activities may increase the brain blood flow improving neural activities leading to improved cognition. Consequently, the effects of an acute bout of moderate intensity aerobic exercise on cortical brain blood oxygenation and its correlation with cognitive color-word Stroop task performance were tested. The Stroop tasks were congruent (color matches word) and incongruent (color does not match word). Prefrontal (PFC) and motor cortex (MC) blood flow was recorded by fNIRS (functional Near-Infrared Spectroscopy) while the human subjects performed the Stroop tasks before and after 30 minutes of exercise or equivalent time of rest (controlling for practice effect of repeating the Stroop task multiple times). It was predicted that PFC blood flow increase after exercise will correlate with increased Stroop interference and decreased cognitive flexibility after an acute bout of aerobic exercise at 70% of maximal Heart Rate (HR). We observed that Stroop interference in aerobic exercise and practice alone (rest) were not significantly (p>0.6) different indicating that exercise did not improve cognition above the learning effect. Increase in blood flow (both neurovascular and neurometabolic coupling) in previously deactivated PFC channels was positively correlated (p<0.05) to increased Stroop interference (worse cognitive speed and accuracy) after an acute bout of aerobic exercise.\n\nHighlightsO_LIDoes moderate intensity aerobic exercise improve cognition?\nC_LIO_LIDoes prefrontal cortex oxygenation correlate with cognition changes after exercise?\nC_LI

neuroscience↗
bioRxiv2017

Age-dependent neurodegeneration and organelle transport deficiencies in mutant TDP43 patient-derived neurons are independent of TDP43 aggregation

TAR DNA-binding protein 43 (TDP43) is a cause of familiar and sporadic amyotrophic lateral sclerosis (ALS). The diverse postulated mechanisms by which TDP43 mutations cause the disease are not fully understood. Human wildtype and TDP43 S393L and G294V mutant spinal motor neuron cultures were differentiated from patient-derived iPSCs. Mutant hTDP43 and wildtype motor neuron cultures did not differ in neuron differentiation capacity during early maturation stage. During aging we detected a dramatic neurodegeneration including neuron loss and pathological neurofilament abnormalities in TDP43 mutant cultures only. Additionally mitochondria and lysosomes of aging spinal motor neurons revealed robust TDP43 mutation dependent abnormal phenotypes in size, shape, speed and motility which all appeared without TDP43 mislocalization or aggregation formation. Furthermore, D-sorbitol - known to induce stress granules and cytoplasmic mislocalization of TDP43 - rescued axonal trafficking phenotypes without any signs of TDP43 mislocalization or aggregation formation. Our data indicate TDP43 mutation-dependent but cytosolic aggregation-independent mechanisms of motor neuron degeneration in TDP43 ALS.

neuroscience↗