Alma Lilia Fuentes-Farías

ACAID as a potential therapeutic approach to modulate inflammation in neurodegenerative diseases

The progressive loss of neurons and inflammation characterizes neurodegenerative diseases. Although the etiology, progression and outcome of different neurodegenerative diseases are varied, they share chronic inflammation maintained largely by central nervous system (CNS)-derived antigens recognized by T cells. Inflammation can be beneficial by recruiting immune cells to kill pathogens or to clear cell debris resulting from the primary insult. However, chronic inflammation exacerbates and perpetuates tissue damage. An increasing number of therapies that attempt to modulate neuroinflammation have been developed. However, so far none has succeeded in decreasing the secondary damage associated with chronic inflammation. A potential strategy to modulate the immune system is related to the induction of tolerance to CNS antigens. In this line, it is our hypothesis that this could be accomplished by using anterior chamber associated immune deviation (ACAID) as a strategy. Thus, we review current knowledge regarding some neurodegenerative diseases and the associated immune response that causes inflammation. In addition, we discuss further our hypothesis of the possible usefulness of ACAID as a therapeutic strategy to ameliorate damage to the CNS.

Speciation, Phenotypic Variation and Plasticity: What Can Endocrine Disruptors Tell Us?

Phenotype variability, phenotypic plasticity, and the inheritance of phenotypic traits constitute the fundamental ground of processes such as individuation, individual and species adaptation and ultimately speciation. Even though traditional evolutionary thinking relies on genetic mutations as the main source of intra- and interspecies phenotypic variability, recent studies suggest that the epigenetic modulation of gene transcription and translation, epigenetic memory, and epigenetic inheritance are by far the most frequent reliable sources of transgenerational variability among viable individuals within and across organismal species. Therefore, individuation and speciation should be considered as nonmutational epigenetic phenomena.

Global DNA methylation, as estimated in blood samples, does not correlate with variations of body condition, anatomical features and hematological parameters in American bullfrogs (Lithobates catesbeianus) kept captive under distinct environmental conditions.

Different levels of Global DNA Methylation (GDM) could have facilitated the emergence of new species, without relying on gene mutations, through promoting ontogenetic phenotypic plasticity. If this assertion was correct, one could expect individuals of the same species living under distinct environmental conditions to be genetically similar, but having different GDM levels and being phenotypically divergent. We tested this presumption by studying the relationship between variability of functional morphological traits and GDM levels in American bullfrog (Lithobates catesbeianus), in green houses located in two geographical sites. Our analyses revealed that body linear morphometry, skull geometry, scaled mass index, packed cell volume and neutrophil counts differed significantly among males and females within and between localities. GDM, nonetheless, was rather similar among sex and locality groups. These results show that levels of GDM, at least under our experimental contexts, does not correlate with functional morphological trait variability.