Social Construction of Technology (SCOT) formed a key component of the ‘new sociology of technology’, which emerged in mid-1980s and heralded the entry of social constructivist theory into the domain of technology from science. A large number of empirical case studies were generated using SCOT methodology in the following three decades, encompassing a wide range of technological artefacts or systems. This essay reviews the trajectory of SCOT as a distinct intellectual tradition in technology studies. First, an attempt is made to appraise and classify the main strands of criticisms against SCOT that have come up over the years. Second, this essay discusses several new conceptual heuristics, which were successively incorporated by the original authors of SCOT, along with the concomitant broadening of analytical units and research questions. We conclude that, while SCOT demonstrated its resilience as a dynamic scholarly tradition and constantly adapted itself to address criticisms through the incorporation of new conceptual tools, the consequent methodological transition had profound implications for SCOT as a theory, somewhat undermining its original agenda and methodological distinctiveness in social studies of technology.

The entangled relationship of brain aging, mitochondrial dysfunction, and amyloid-β peptide (Aβ₄₂) toxicity occupies the center stage in the pathogenesis of Alzheimer's disease (AD). The present study examines some of the toxic effects of Aβ₄₂ on brain mitochondria and provides evidence that aged brain mitochondria are significantly more vulnerable to Aβ₄₂ toxicity. In particular, the study has shown that the aggregated, but not the monomeric, form of Aβ₄₂ in varying concentrations (10-40 μM) during in vitro incubation causes a loss of mitochondrial membrane potential, a decrease in phosphorylation capacity and ATP synthesis, and the release of cytochrome c from the mitochondria but without any noticeable change in the activities of respiratory chain complexes. Such effects of Aβ₄₂ are strikingly more conspicuous on aged rat (22-24 months) brain mitochondria compared to that on brain mitochondria of young rats (4-6 months). More interestingly is the observation that in contrast to young rat brain mitochondria, a significantly higher level of Aβ₄₂ remains associated with aged brain mitochondria under basal incubation condition as well as after exposure to exogenously added peptide. Extrapolated to an in vivo scenario, the results have clear implications in AD pathogenesis and also partly explain why brain aging is a dominant risk factor for this disease condition.