Objective: To use digital histology in a large autopsy cohort of Lewy Body Disorder (LBD) patients with dementia to test the hypotheses that co-occurring Alzheimer’s disease (AD) pathology impacts the anatomic distribution of α-synuclein (SYN) pathology and that co-occurring neocortical tau pathology in LBD associates with worse cognitive performance and occurs in a pattern differing from AD. Methods: Fifty-five autopsy-confirmed LBD (PDD: 36, DLB:19) patients and 25 AD patients were studied. LBD patients were categorized as having moderate/severe AD co-pathology (SYN+AD=20) or little/no AD co-pathology (SYN-AD=35). Digital measures of tau, Aβ, and SYN histopathology in neocortical and subcortical/limbic regions were compared between groups and related to antemortem cognitive testing. Results: SYN burden was higher in SYN+AD than SYN-AD in each neocortical region (F(1,54)=5.6–6.0,p<0.02) but was equivalent in entorhinal cortex and putamen (F(1,43–49)=0.7–1.7,p>0.2). SYN+AD performed worse than SYN-AD on a temporal-lobe mediated naming task (t(27)=2.1,p=0.04). Antemortem cognitive test scores inversely correlated with tau burden (r=−0.39 to −0.68,p<0.05). AD had higher tau than SYN+AD in all regions (F(1,43)=12.8–97.2,p<.001); however, SYN+AD had a greater proportion of tau in the temporal neocortex than AD, (t(41)=2.0,p<.05) whereas AD had a greater proportion of tau in the frontal neocortex than SYN+AD (t(41)=3.3,p<0.002). SYN+AD had similar severity and distribution of neocortical Aβ compared to AD (F(1,40–43)=1.6–2.0,p>.1). Interpretation: LBD patients with AD co-pathology harbor greater neocortical SYN pathology. Regional tau pathology relates to cognitive performance in LBD dementia, and its distribution may diverge from pure AD. Tau co-pathology contributes uniquely to the heterogeneity of cognitive impairment in LBD.

Fiber-based coalescers are widely used to accumulate droplets from aerosols and emulsions, where the accumulated droplets are typically removed by gravity or shear. This Letter reports self-propelled removal of drops from a hydrophobic fiber, where the surface energy released upon drop coalescence overcomes the drop-fiber adhesion, producing spontaneous departure that would not occur on a flat substrate of the same contact angle. The self-removal takes place above a threshold drop-to-fiber radius ratio, and the departure speed is close to the capillary-inertial velocity at large radius ratios.

Objective: To measure postmortem burden of frontotemporal lobar degeneration (FTLD) with TDP-43 (FTLD-TDP) or tau (FTLD-Tau) proteinopathy across hemispheres in primary progressive aphasia (PPA) using digital histopathology and to identify clinicopathological correlates of these distinct proteinopathies. Methods: In an autopsy cohort of PPA (FTLD-TDP = 13, FTLD-Tau = 14), we analyzed laterality and regional distribution of postmortem pathology, quantified using a validated digital histopathological approach, in available brain tissue from up to 8 cortical regions bilaterally. We related digital pathology to antemortem structural neuroimaging and specific clinical language features. Results: Postmortem cortical pathology was left-lateralized in both FTLD-TDP (beta = −0.15, standard error [SE] = 0.05, p = 0.007) and FTLD-Tau (beta = −0.09, SE = 0.04, p = 0.015), but the degree of lateralization decreased with greater overall dementia severity before death (beta = −8.18, SE = 3.22, p = 0.015). Among 5 core pathology regions sampled, we found greatest pathology in left orbitofrontal cortex (OFC) in FTLD-TDP, which was greater than in FTLD-Tau (F = 47.07, df = 1,17, p < 0.001), and in left midfrontal cortex (MFC) in FTLD-Tau, which was greater than in FTLD-TDP (F = 19.34, df = 1,16, p < 0.001). Postmortem pathology was inversely associated with antemortem magnetic resonance imaging cortical thickness (beta = −0.04, SE = 0.01, p = 0.007) in regions matching autopsy sampling. Irrespective of PPA syndromic variant, single-word comprehension impairment was associated with greater left OFC pathology (t = −3.72, df = 10.72, p = 0.004) and nonfluent speech with greater left MFC pathology (t = −3.62, df = 12.00, p = 0.004) among the 5 core pathology regions. Interpretation: In PPA, FTLD-TDP and FTLD-Tau have divergent anatomic distributions of left-lateralized postmortem pathology that relate to antemortem structural imaging and distinct language deficits. Although other brain regions may be implicated in neural networks supporting these complex language measures, our observations may eventually help to improve antemortem diagnosis of neuropathology in PPA.

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Reliable cerebral rSO2 readings before, during, and after shunt tap were demonstrated. Left cerebral rSO2 changes from before to after shunt tap were more predictive for shunt malfunction location than right cerebral rSO2 changes. Observing cerebral rSO2 changes in relationship to shunt tap represents a potential surrogate in measuring cerebral pressures and blood flow changes after cerebral spinal fluid drainage. Significantly greater cerebral rSO2 changes occur for distal malfunction versus proximal malfunction after shunt tap, indicating its potential as an adjunct tool for detecting shunt malfunction type.