Neolithic and Early Bronze Age anthropomorphic figurines from the Aegean have hitherto constituted separate fields of study. The present article proposes a uniform methodological strategy and theoretical perspective, aimed at uniting both sets of figurines to explore social dynamics through the study of gender. The main ideas discussed focus on the complex ways in which gender identities were constructed, the mechanisms of power negotiation, and the ways in which the physical and cultural body constituted an axis on which prehistoric societies organised themselves at a socio-economic and ideological level. The analysis exposes some of the biases that have coloured previous unilinear interpretations, and calls for a critical review of traditional social models, according to which the 'egalitarian' Neolithic was followed by the rise of patriarchy in the EBA.

The intensity of muscle contraction, and therefore movement vigour, needs to be adaptable to enable complex motor behaviors. This can be achieved by adjusting the properties of motor neurons, which form the final common pathway for all motor output from the central nervous system. Here we identify novel roles for a neuropeptide, Cocaine and Amphetamine Regulated Transcript (CART), in the control of movement vigour. We reveal distinct, but parallel mechanisms by which CART and acetylcholine, both released at C bouton synapses on motor neurons, selectively amplify the output of subtypes of motor neurons that are recruited during intense movement. We find that mice with broad genetic deletion of CART or selective elimination of acetylcholine from C boutons exhibit deficits in behavioral tasks that require higher levels of motor output. Overall, these data uncover novel spinal modulatory mechanisms that control movement vigour to support movements that require a high degree of muscle force.

This article is based on an EAA session in Kiel in 2021, in which thirteen contributors provide their response to Robb and Harris's (2018) overview of studies of gender in the European Neolithic and Bronze Age, with a reply by Robb and Harris. The central premise of their 2018 article was the opposition of ‘contextual Neolithic gender’ to ‘cross-contextual Bronze Age gender’, which created uneasiness among the four co-organizers of the Kiel meeting. Reading Robb and Harris's original article leaves the impression that there is an essentialist ‘Neolithic’ and ‘Bronze Age’ gender, the former being under-theorized, unclear, and unstable, the latter binary, unchangeable, and ideological. While Robb and Harris have clearly advanced the discussion on gender, the perspectives and case studies presented here, while critical of their views, take the debate further, painting a more complex and diverse picture that strives to avoid essentialism.

Amyotrophic Lateral Sclerosis (ALS) is the most common motor neuron disease and is clinically defined by the degeneration of upper and lower motor neurons, leading to paralysis and premature death. 10% of ALS patients suffer from the familial form of the disease and research has revealed a number of responsible mutations in specific genes and loci. Transgenic mouse models carrying human ALS related mutations have been generated for the study of the mechanisms involved in the disease pathogenesis and putative therapies. Mutations in the Cu/ Zn superoxide dismutase 1 (SOD1) gene, accounting for 20% of fALS and up to 5% of sALS, were the first identified to be involved in the disease. In this review, we focus on the first transgenic model used, the SOD1 mouse, which recapitulates many symptoms of the human ALS pathology. SOD1 mouse models have been extensively studied in basic and translational research, in order to unravel the underlying mechanisms, the early signs of the disorder and potential therapeutic interventions. In basic research this model has provided valuable information about ALS causes and progression. In translational research, encouraging results have emerged, but the need for better design of clinical trials is evident. This review presents the impact of the SOD1 mouse models in ALS investigation.

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