Particular features of gonadal maturation and size at first maturity in Atrina maura

The gonadal maturation of Atrina maura was examined by means of histological analysis and quantitative criteria. Particular features not previously described for this species are reported in this study: in both males and females the undifferentiated stage is absent and there is massive gamete resorption when the seawater temperature reaches 25°C; in males, there is continuous spawning concurrent with other gonadal development stages and the adipogranular cells surrounding the acini walls decrease with testis ripeness, which suggests they play an energetic role. Atresia displayed two stages: cytoplasmic structures with oocyte degeneration and digestion by hemocytes. The oocyte diameter was larger than that reported for cultured specimens. Size at first maturity was reached at 23.3 cm in shell height (SH) (12.2 cm in shell length, SL) in females and 22.8 cm SH (12.0 cm SL) in males

Ultrastructural and Histological Study of Oogenesis and Oocyte Degeneration in the PenshellAtrina maura(Bivalvia: Pinnidae)

The successive stages of oogenesis and the changes involved in the oocyte degeneration process in the penshell Atrina maura were examined using light and transmission electron microscopy. The ovarian maturation process is asynchronous, as oocytes at different developmental stages can be found simultaneously. Oocytes develop from oogonia and then undergo three distinct stages of oogenesis: previtellogenesis, vitellogenesis and postvitellogenesis with mature oocytes. Atrina maura displays a solitary oogenesis type, in which follicular cells become associated with oocytes from the earliest stages of development and seem to play an integral role in vitellogenesis. The cytoplasm of vitellogenic oocytes contains numerous whorls of rough endoplasmic reticulum and Golgi bodies, suggesting that auto-synthetic vitellogenesis may occur in this species. In addition, the degeneration process of postvitellogenic oocytes triggered by a seasonal increase in water temperature (> 25°C) is described

Amyloid-β-independent regulators of tau pathology in Alzheimer disease

The global epidemic of Alzheimer disease (AD) is worsening, and no approved treatment can revert or arrest progression of this disease. AD pathology is characterized by the accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the brain. Genetic data, as well as autopsy and neuroimaging studies in patients with AD, indicate that Aβ plaque deposition precedes cortical tau pathology. Because Aβ accumulation has been considered the initial insult that drives both the accumulation of tau pathology and tau-mediated neurodegeneration in AD, the development of AD therapeutics has focused mostly on removing Aβ from the brain. However, striking preclinical evidence from AD mouse models and patient-derived human induced pluripotent stem cell models indicates that tau pathology can progress independently of Aβ accumulation and arises downstream of genetic risk factors for AD and aberrant metabolic pathways. This Review outlines novel insights from preclinical research that implicate apolipoprotein E, the endocytic system, cholesterol metabolism and microglial activation as Aβ-independent regulators of tau pathology. These factors are discussed in the context of emerging findings from clinical pathology, functional neuroimaging and other approaches in humans. Finally, we discuss the implications of these new insights for current Aβ-targeted strategies and highlight the emergence of novel therapeutic strategies that target processes upstream of both Aβ and tau