Abstract. Corema album (Ericaceae), "Camarinhas", endemic of the Atlantic dunes of the Iberian Peninsula has the possibility to become a new niche berry crop. Considering the agronomic and market possibilities for this species, the initial research step is the development of a seed germination protocol. We characterized C. album populations along its biogeographical area. The results show that different seeds characteristics differ significantly between sites. We also tested the effect of pretreatments on the germination of C. album seeds (subsp. album) from Duna de Quiaios in 2011, from Comporta in 2011 and Aldeia do Meco in 2011 and in 2012. The results show that there is site-to-site variation in the same year and year-to-year variation in a particular site in percentage of germinated seeds. Acid scarification (30, 60 and 120 minutes) followed by 1000 ppm of gibberellic acid was the most effective pretreatment in breaking dormancy of C. album and this pretreatment promote the best germination from seeds collected from Aldeia do Meco 2011 (30.3%) after 175 days. Our results suggest that the seeds had physiological dormancy. Considering the 2800 seeds collected: 54.5% ruptured the seed coat and 7.7% germinated.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with short life expectancy and no effective therapy. We previously identified upregulated miR-124 in NSC-34-motor neurons (MNs) expressing human SOD1-G93A (mSOD1) and established its implication in mSOD1 MN degeneration and glial cell activation. When anti-miR-124-treated mSOD1 MN (preconditioned) secretome was incubated in spinal cord organotypic cultures from symptomatic mSOD1 mice, the dysregulated homeostatic balance was circumvented. To decipher the therapeutic potential of such preconditioned secretome, we intrathecally injected it in mSOD1 mice at the early stage of the disease (12-week-old). Preconditioned secretome prevented motor impairment and was effective in counteracting muscle atrophy, glial reactivity/dysfunction, and the neurodegeneration of the symptomatic mSOD1 mice. Deficits in corticospinal function and gait abnormalities were precluded, and the loss of gastrocnemius muscle fiber area was avoided. At the molecular level, the preconditioned secretome enhanced NeuN mRNA/protein expression levels and the PSD-95/TREM2/IL-10/arginase 1/MBP/PLP genes, thus avoiding the neuronal/glial cell dysregulation that characterizes ALS mice. It also prevented upregulated GFAP/Cx43/S100B/vimentin and inflammatory-associated miRNAs, specifically miR-146a/miR-155/miR-21, which are displayed by symptomatic animals. Collectively, our study highlights the intrathecal administration of the secretome from anti-miR-124-treated mSOD1 MNs as a therapeutic strategy for halting/delaying disease progression in an ALS mouse model.