Neurogenic niches are important spots into the brain in which neural stem cells and other homeostatic populations harbour, and in which neurogenesis takes place. One of their well-renown limits is represented by the fact that, as years pass by, niches become less-functional, and neural regeneration becomes less efficient. RNA sequencing-based single-cell analysis, performed by Dulken and collaborators, individuated, for the first time, a clonally-expanded population of CD8+ T cells in older mice that might be responsible of loss of efficiency of the neural progenitors in the niches. These lymphocytes display a different transcriptomic fingerprint from those found in the periphery, they are almost absent in younger animals and express gamma-interferon (IFNg), by means of which they seem to be able to suppress proliferation in the interferon-responding neurons of the neurogenic niches.
Lack of remyelination and microglial activation in the central nervous system (CNS) are common features of several neurodegenerative diseases (e.g. multiple sclerosis, amiotrophic lateral sclerosis, spinal cord injury). On the other end, effective regeneration of the axonal myelin sheath strongly depends on the capacity of CNS-resident microglia of undergoing a phenotypical transition during which pro-inflammatory markers (such as iNOS, TNF-alpha and CCL2) are downregulated and pro-resolving/pro-regenerative ones are expressed (Arg-1, CD206, IGF1). Lack of this conversion leads to impaired regeneration and remyelination, bu the causes that lead to this event are basically unknown. In this paper, Amy Lloyd and colleagues, investigated the molecular mechanisms that underlie the regeneration of the CNS lesions mediated by the functional transition of microglia and saw that, quite interestingly, remyelination depends on the necroptosis of pro-inflammatory microglia in the early moments of the lesion and on the consequent repopulation of the lesioned site of pro-regenerative microglial phenotypes.
Mammal brains are inhabited by a myriad of myelod cells, a good part of which is represented by resident parenchymal microglia, the homeostatic role of which, in the brain, has been abundantly investigated in the last decades. On the other hand, other brain-resident myeloid lineages, usually located at the outer interface regions of the central nervous system (CNS) have still been poorly characterized, and their involvement in brain homeostasis largely unknown. In this paper, recently published by Hannah Van Hove and collaborators on Nature Neuroscience, the authors characterized the trascriptional fingerprint, phenotype and ontogeny of monocyte subsets that reside in different non-parenchymal brain compartments.
I believe that there is at least one moment (to say the least) in the life of a scientist in which he thought to his data as a sort of superposition between "statistically significant" and something more like "well... there's definitelly a trend there", the latter definition often used when the difference observed in the data sets didn't reach the statistical threshold to be deemed "non-casual". When the second case occurs, the only conclusion is that the two (or more) mean values belong to samples of the same population that happened to be different only by sheer chance, and not due to our experimental hypothesis. Usually, in bio-medical sciences, this threshold is represented by alpha=0.05 and, quite unfortunately it has gradually become the magical door that divides undignified results from striking discoveries -some sort of holy grail of scientific literature, and has transformed several scientifical endeavors in trivial search for a p-value that was lower of 0.05. Things, however, might be mature enough for a "surgical strike on thoughtless testing of statistical significance".
Just a few days ago, the Cambridge team led by Ravindra Gupta announced that they had been able to eliminate HIV virus in a patient that had received a bone marrow transplant from a donor that carried two mutated copies of CCR5 -a mutation that occurs in around 1% of european descent- that confers HIV immunity to the host. The treated patient stopped taking antiretroviral drugs in the past 18 months after the transplant and, quite importantly, represents the second case of succesful HIV-treating transplant in recent years, the first having been reported in 2009. Interestingly, the idea behind a stem cell-based treatment came, for both patients, from the necessity of a bone marrow transplant as a treatment for a blood cancer that did not respond to chemotherapy; however, rather than chosing any compatible donor, Dr. Gupta opted for a patient with a double mutation for CCR5.
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