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Abstract: The Central Atlantic Magmatic Province (CAMP), one of the largest known flood basalt provinces formed in the Phanerozoic, is associated with the pre-rift stage of the Atlantic Ocean at the Triassic–Jurassic boundary ca. 200 Ma. Paleomagnetic sampling targeted packages of CAMP lava flows in Morocco''s High Atlas divided into four basic units (the lower, intermediate, upper, and recurrent units) from sections identified on the basis of field observations and geochemistry. Oriented cores were demagnetized using both alternating field (AF) and thermal techniques. Paleomagnetic results reveal wholly normal polarity interrupted by at least one brief reversed chron located in the intermediate unit, and reveal distinct pulses of volcanic activity identified by discrete changes in declination and inclination. These variations in magnetic direction are interpreted as a record of secular variation, and they may provide an additional correlative tool for identification of spatially separated CAMP lava flows within Morocco. 40Ar/39Ar analyses of Moroccan CAMP lavas yield plateau ages indistinguishable within 2σ error limits, sharing a weighted mean age of 199.9±0.5 Ma (2σ), reinforcing the short-lived nature of these eruptions despite the presence of sedimentary horizons between them. Correlation of our sections with the E23n, E23r, E24 sequence reported in the Newark basin terrestrial section and St. Audrie''s Bay marine section is suggested. Brief volcanism in sudden pulses is a potential mechanism for volcanic-induced climatic changes and biotic disruption at the Triassic–Jurassic boundary. Combination of our directional group (DG) poles yields an African paleomagnetic pole at 200 Ma of λ(°N)=73.0°, ϕ(°E)=241.3° (Dp=5.0°, Dm=18.5°). [Copyright &y& Elsevier]

In the past two decades, genetic studies of familial forms of Parkinson's disease (PD) have shown evidence that PD has a significant genetic component. Indeed, 12 genes are strongly involved in PD causality, three of them having dominant inheritance and 9 causing early-onset autosomal recessive forms, including 3 with a typical PD and 6 with an atypical parkinsonism. The aim of this study was to determine the genetic basis of familial PD in Moroccan patients. We selected 18 Moroccan index case with familial forms of PD. Patients were first screened for exon-rearrangements by MLPA kit. They were then analyzed by gene panel next-generation sequencing (NGS). Functional variants with minor allele frequencies < 0.5% in public databases were considered potential candidate variants to PD. In the 18 PD patients with a positive family history that were analyzed, MLPA assays identified PRKN deletions in two patients: a homozygous exon 3-5 deletion and a heterozygous exon 4 deletion. Sixteen rare SNV were identified by NGS, four of them were novel. Seven mutations were categorized as pathogenic, five as likely pathogenic, two to be of uncertain significance, and 3 were predicted to be likely benign but may give a weaker pathogenic effect and could contribute to PD since they were found in late-onset PD patients. Rare or novel mutations that could be related to the disease were identified in 72% of these patients (13/18), including nine with bi-allelic pathogenic/likely pathogenic variants in genes causing recessive PD, particularly PRKN and PINK1. Mutations in genes with dominant inheritance were found in 4/18 patients (22%).