We calculate the evolution of heavy-element abundances from C to Zn in the solar neighborhood, adopting our new nucleosynthesis yields. Our yields are calculated for wide ranges of metallicity (Z ¼ 0YZ ) and the explosion energy (normal supernovae and hypernovae), based on the light-curve and spectra fitting of individual supernovae. The elemental abundance ratios are in good agreement with observations. Among the -elements, O, Mg, Si, S, and Ca show a plateau at ½Fe/H P À1, while Ti is underabundant overall. The observed abundance of Zn (½Zn/Fe $ 0) can be explained only by the high-energy explosion models, as it requires a large contribution of hypernovae. The observed decrease in the odd-Z elements (Na, Al, and Cu) toward low ½Fe/H is reproduced by the metallicity effect on nucleosynthesis. The iron-peak elements (Cr, Mn, Co, and Ni) are consistent with the observed mean values at À2:5 P ½Fe/H P À1, and the observed trend at the lower metallicity can be explained by the energy effect. We also show the abundance ratios and the metallicity distribution functions of the Galactic bulge, halo, and thick disk. Our results suggest that the formation timescale of the thick disk is $1Y3 Gyr.

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are associated with loss of nuclear TDP-43. Here we identify that TDP-43 regulates expression of the neuronal growth-associated factor stathmin-2. Lowered TDP-43 levels, which reduce its binding to sites within the first intron of stathmin-2 pre-mRNA, uncover a cryptic polyadenylation site whose utilization produces a truncated, non-functional mRNA. Reduced stathmin-2 expression is found in neurons trans-differentiated from patient fibroblasts expressing an ALS-causing TDP-43 mutation, in motor cortex and spinal motor neurons from sporadic ALS patients and familial ALS patients with expansion in C9orf72, and in induced pluripotent stem cell (iPSC)-derived motor neurons depleted of TDP-43. Remarkably, while reduction in TDP-43 is shown to inhibit axonal regeneration of iPSC-derived motor neurons, rescue of stathmin-2 expression restores axonal regenerative capacity. Thus, premature polyadenylation-mediated reduction in stathmin-2 is a hallmark of ALS/FTD that functionally links reduced nuclear TDP-43 function to enhanced neuronal vulnerability.

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