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opencc-zeroApr 2021View details →

Latent atrophy factors related to phenotypical variants of posterior cortical atrophy

Objective: To determine whether atrophy relates to phenotypical variants of posterior cortical atrophy (PCA) recently proposed in clinical criteria; dorsal, ventral, dominant-parietal and caudal, we assessed associations between latent atrophy factors and cognition. Methods: We employed a data-driven Bayesian modelling framework based on latent Dirichlet allocation to identify latent atrophy factors in a multi-center cohort of 119 individuals with PCA (age:64±7, 38% male, MMSE:21±5, 71% amyloid-β-positive, 29% amyloid-β status unknown). The model uses standardized gray matter density images as input (adjusted for age, sex, intracranial volume, field-strength and whole-brain gray matter volume) and provides voxelwise probabilistic maps for a predetermined number of atrophy factors, allowing every individual to express each factor to a degree without a-priori classification. Individual factor expressions were correlated to four PCA-specific cognitive domains (object-perception, space-perception, non-visual/parietal functions and primary visual processing) using general linear models. Results: The model revealed four distinct yet partially overlapping atrophy factors; right-dorsal, right-ventral, left-ventral, and limbic. We found that object-perception and primary visual processing were associated with atrophy that predominantly reflects the right-ventral factor. Furthermore, space-perception was associated with atrophy that predominantly represents the right-dorsal and right-ventral factors. However, individual participant profiles revealed that the vast majority expressed multiple atrophy factors and had mixed clinical profiles with impairments across multiple domains, rather than displaying a discrete clinical-radiological phenotype. Conclusion: Our results indicate that particular brain-behavior networks are vulnerable in PCA, but most individuals display a constellation of affected brain-regions and symptoms, indicating that classification into four mutually exclusive variants is unlikely to be clinically useful.

opencc-zeroMar 2022View details →

Supplementary Data to: Mediterranean diet, Alzheimer's disease biomarkers and brain atrophy in old age

Objective: To determine if following a Mediterranean-like diet (MeDi) relates to cognitive functions and in vivo biomarkers for Alzheimer's disease (AD), we analyzed cross-sectional data from the German Longitudinal Cognitive Impairment and Dementia Study Method: The sample (n=512, mean age: 69.5±5.9 years) included 169 cognitively normal participants and subjects at higher AD risk (53 AD relatives, 209 SCD and 81 MCI). We defined MeDi adherence based on the Food Frequency Questionnaire. Brain volume outcomes were generated via voxel-based morphometry on T1-MRI and cognitive performance with an extensive neuropsychological battery. AD-related biomarkers (Aβ42/40 ratio, pTau181) in cerebrospinal fluid were assessed in n=226 individuals. We analyzed the associations between MeDi and the outcomes with linear regression models controlling for several covariates. Additionally, we applied hypothesis-driven mediation and moderation analysis. Results: Higher MeDi adherence related to larger mediotemporal gray matter volume (p<0.05 FWE corrected), better memory (β±SE = 0.03 ± 0.02; p=0.038), and less amyloid (Aβ42/40 ratio, β±SE = 0.003 ± 0.001; p=0.008) and pTau181 pathology (β±SE = -1.96±0.68; p=0.004). Results were consistent correcting for ApoE- ε4 status. Mediotemporal volume mediated the association between MeDi and memory (40% indirect mediation). Finally, MeDi favorably moderated the associations between Aβ42/40 ratio, pTau181 and mediotemporal atrophy. Conclusion: Our findings corroborate the view of MeDi as a protective factor against memory decline and mediotemporal atrophy. Importantly, they suggest that these associations might be explained by a decrease of amyloidosis and tau-pathology. Longitudinal and dietary intervention studies should further examine this conjecture and its treatment implications.

FIGURE 9 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 9. Key apomorphic characters of Austrocheirus isasii. Metacarpal III of Dilophosaurus wetherilli (A), Ceratosaurus nasicornis (B), and Austrocheirus isasii (C). Distal tibia of Dilophosaurus wehterilli (D), Velocisaurus uniqus (E), Austrocheirus isasii (F), and Majungasaurus (G). Character 104 (1): poor development of the metacarpal III flexor fossa, Character 106 (1): metacarpal III with dorsal margin of the distal articular condyles protruded directly above the collateral ligament pits. Character 107 (1): asymmetric distal condyles of metacarpal III. Character 115 (1): tibia with the scar of the ascending process of the astragalus bearing a vertical ridge. Character 116 (1) distal end of the tibia with a vertical astragalar facet. Not to scale. (A based on UCMP 37302; B based on USNM 4735; C and F based on MPM-PV 10003; D based on UCMP 77270; E based on MUCPv 41; G based on Carrano 2007).

FIGURE 8 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 8. Strict consensus tree depicting the phylogenetic relationships of Austrocheirus isasii among ceratosaurian theropods. Numbers separated by a backslash are bootstrap frequencies (resampling analysis carried on with 5000 replications), absolute frequencies on the left and frequency differences (GC) on the right. Isolated numbers at each node are decay indexes. Abbreviations: Abeli, Abelisauroidea; Aver, Averostra.

FIGURE 7 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 7. Internal structure of metacarpal III of Austrocheirus isasii. High-resolution photograph of the cortical bone and part of the spongy bone on the lateroventral corner of the shaft. The arrows indicate LAGs. Abbreviations: cb, cortical bone; EFS, external fundamental system; hdo, high density of osteons; ldo, low density of osteons; sb, spongy bone; t, trabecula. Scale bar equals 5 mm.

FIGURE 6 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 6. Caudal vertebrae of Austrocheirus isasii. Neural arches in posterior (A, D, G), ventral (B, E, H), left lateral (C, F), and right lateral (I) views. Centra in anterior/posterior (J, K) and side (L) views. Abbreviations: mn, median notch; nc, neural canal; ns, neural spine; poz, postzygapophysis. Scale bars equal 2 cm.

FIGURE 4 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 4. Distal end of left tibia of Austrocheirus isasii in anterior (A, B), lateral (C), posterior (D), medial (E), proximal (F), and distal (G) views. Abbreviations: asap, anterior surface for the reception of the ascending process of the astragalus; fap, facet for the reception of the ascending process of the astragalus; ldp, lateral distal process; mdp, medial distal process; mvr, median vertical ridge; ob, oblique ridge. Scale bar equals 5 cm.

FIGURE 3 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 3. Manual elements of Austrocheirus isasii. Metacarpal III in medial (A), lateral (B), dorsal (C, D), ventral (E), proximal (F), and distal (G) views. Proximal phalanx of digit III in medial (H, I), lateral (J), distal (K), and ventral (L) views. Abbreviations: af, articular facet for metacarpal II; ctf, collateral tendinal fossa; dlp, dorsal ligament pit; ldc, lateral distal condyle; mdc, medial distal condyle; mig, median intercondylar groove; paf, proximal articular facet; pdm, projected dorsal margin. Scale bar equals 2 cm for A–G and 1 cm for H–L.

FIGURE 2 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 2. Unique combination of features of Austrocheirus isasii compared with other basal theropods. Metacarpals III in lateral views of Austrocheirus (A), Dilophosaurus (B), and Allosaurus (C); tibiae in distal views of Austrocheirus (D), Berberosaurus (E), Velocisaurus (F), and Masiakasaurus (G); metatarsals III in medial views of Austrocheirus (H) and Masiakasaurus (I); and pedal phalanges in side views of Austrocheirus (J), Elaphrosaurus (K), Velocisaurus (L), and Majungasaurus (M). Note the presence of the following autapomorphies in Austrocheirus: metacarpal III with a posteriorly tapering shaft and a posteriorly diplaced collateral fossa (A–C); pedal phalanges with a dorsal tubercle above the collateral fossa (J–M). Abbreviations: adr, absence of dorsal ridge; ccf, centrally located collateral fossa; ccpl, concave posterolateral margin; cvpl, convex posterolateral margin; dr, dorsal ridge; hs, dorsoventrally homogeneous shaft; lt, large tuber; pdf, proximally displaced collateral fossa; pts, proximally tapering shaft; st, small tuber. Not to scale. (B based on UCMP 37302; C based on Madsen 1976; E based on Allain et al. 2007; F, L based on MUCPv 41; G, I based on Carrano et al. 2002; K based on MB unnumbered; M based on Carrano 2007).

FIGURE 5 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 5. Pedal elements of Austrocheirus isasii. Left metatarsal III in medial (A), lateral (B), dorsal (C), ventral (D), proximal (G), and distal (H) views. Metatarsal II in cross-section (E) and ventral (F) views. Several pedal phalanges in side (I–K, M) and distal (L) views. Abbreviations: as, articular surface; ctf, collateral tendinal fossa; dlp, dorsal ligament pit; dr, dorsal ridge; mig, median intercondylar groove; vt, ventral tuber. Scale bars equal 5 cm for A–H and 1 cm for I– M.

FIGURE 1 in An abelisauroid dinosaur with a non-atrophied manus from the Late Cretaceous Pari Aike Formation of southern Patagonia

FIGURE 1. Map of the locality in the Pari Aike Formation that has yielded the holotype of Austrocheirus isasii (modified from Novas et al. 2005). The large black bone indicates the Hoyada Arroyo Seco locality and provenance of Austrocheirus and the small grey bone depicts the provenance of Talenkauen and Orkoraptor.

opencc-zeroDec 2023View details →

Data for: Global frequency analyses of canine progressive rod-cone degeneration–progressive retinal atrophy and collie eye anomaly using commercial genetic testing data

Hundreds of genetic variants associated with canine traits and disorders have been identified, with commercial tests offered. However, the geographic distributions and changes in allele and genotype frequencies over prolonged, continuous periods of time are lacking. This study utilized a large set of genotypes from dogs tested for the progressive rod-cone degeneration–progressive retinal atrophy (prcd-PRA) G>A missense PRCD variant (n = 86,667) and the collie eye anomaly (CEA)-associated NHEJ1 deletion (n = 33,834) provided by the commercial genetic testing company (Optigen/Wisdom Panel, Mars Petcare Science & Diagnostics). These data were analyzed using the chi-square goodness-of-fit test, time-trend graphical analysis, and regression modeling in order to evaluate how test results changed over time. The results span fifteen years, representing 82 countries and 67 breeds/breed mixes. Both diseases exhibited significant differences in genotype frequencies (p = 2.7 × 10−152 for prcd-PRA and 0.023 for CEA) with opposing graphical trends. Regression modeling showed time progression to significantly affect the odds of a dog being homozygous or heterozygous for either disease, as do variables including breed and breed popularity. This study shows that genetic testing informed breeding decisions to produce fewer affected dogs. However, the presence of dogs homozygous for the disease variant, especially for prcd-PRA, was still observed fourteen years after test availability, potentially due to crosses of unknown carriers. This suggests that genetic testing of dog populations should continue.

opencc-zeroNov 2021View details →

Association of gray matter atrophy patterns with clinical phenotype and progression in multiple sclerosis

Objectives. Grey matter (GM) involvement is clinically relevant in multiple sclerosis (MS). Using source-based morphometry (SBM), we characterized GM atrophy and its 1-year evolution across different MS phenotypes. Methods. Clinical and MRI data were obtained at 8 European sites from 170 healthy controls (HCs) and 398 MS patients (34 clinically isolated syndromes [CIS], 226 relapsing-remitting [RR], 95 secondary progressive [SP] and 43 primary progressive [PP] MS). Fifty-seven HC and 144 MS underwent 1-year follow-up. Baseline GM loss, atrophy progression and correlations with disability and 1-year clinical worsening were assessed. Results. SBM identified 26 cerebellar, subcortical, sensory, motor and cognitive GM components. GM atrophy was found in MS vs HC in almost all components (p=range<0.001-0.04). Compared to HCs, CIS patients showed circumscribed subcortical, cerebellar, temporal and salience GM atrophy, while RRMS patients exhibited widespread GM atrophy. Cerebellar, subcortical, sensorimotor, salience and fronto-parietal GM atrophy was found in PPMS patients vs HCs, and SPMS vs RRMS. At 1-year, 21 (15%) patients had clinically worsened. GM atrophy progressed in MS in subcortical, cerebellar, sensorimotor, and fronto-temporo-parietal components. Baseline higher disability was associated (R2=0.65) with baseline lower normalized brain volume (beta=-0.13, p=0.001), greater sensorimotor GM atrophy (beta=-0.12, p=0.002) and longer disease duration (beta=0.09, p=0.04). Baseline normalized GM volume (odds ratio=0.98, p=0.008) and cerebellar GM atrophy (odds ratio=0.40, p=0.01) independently predicted clinical worsening (area-under-the-curve=0.83). Conclusion. GM atrophy differed across disease phenotypes and progressed at 1-year in MS. In addition to global atrophy measures, sensorimotor and cerebellar GM atrophy explained baseline disability and clinical worsening.

opencc-by-4.0Jul 2022View details →

Coding and noncoding genes involved in atrophy and compensatory muscle growth in Nile Tilapia

Electronic Supplementary Material: Supplementary Table S1;Supplementary Table S2;Supplementary Table S3

opencc-by-4.0Nov 2019View details →

Resistance exercise with anti-inflammatory foods attenuate skeletal muscle atrophy induced by chronic inflammation

Supplemental figures and table of "Resistance exercise with anti-inflammatory foods attenuate skeletal muscle atrophy induced by chronic inflammation".

opencc-by-4.0Sep 2021View details →

dataset related to article "Dysregulation of Muscle-Specific MicroRNAs as Common Pathogenic Feature Associated with Muscle Atrophy in ALS, SMA and SBMA: Evidence from Animal Models and Human Patients"

CINZIA CAGNOLI 0000-0001-6863-6687, MICHELA TAIANA 0000-0001-8257-8831, MONICA NIZZARDO 0000-0001-5447-0882, STEFANIA CORTI 0000-0001-5425-969X, VIVIANA PENSATO 0000-0001-9798-2669, ANNA VENERANDO <a href="https://orcid.org/0000-0002-7489-1833">0000-0002-7489-1833</a>, CINZIA GELLERA <a href="https://orcid.org/0000-0002-3582-665X">0000-0002-3582-665X</a>, SILVIA FENU 0000-0002-5233-6580, DAVIDE PAREYSON 0000-0001-6854-765X, RICCARDO MASSON 0000-0002-9311-452X, LORENZO MAGGI 0000-0002-0932-5173, ELEONORA DALLA BELLA 0000-0001-6267-9651, GIUSEPPE LAURIA 0000-0001-9773-020X, RENATO MANTEGAZZA 0000-0002-9810-5737, PIA BERNASCONI 0000-0003-0869-2104, ANGELO POLETTI 0000-0002-8883-0468, SILVIA BONANNO 0000-0002-8823-6821, STEFANIA MARCUZZO 0000-0001-6893-6372.