28 (For details of Leiden students see Molhuysen29 and for Dutch and German graduates Manfred Komorowski’s book.26) Table 5 Place of graduation of Jewish physicians in the Netherlands: 1607–1740. Settled in Amsterdam, the place of study for those

Jewish practitioners who wished for more than the license from the Guild of Surgeons or the Amsterdam magistrates to practice, the most popular university choices were Leiden and Utrecht. Eighty-six Jewish physicians were identified practicing in the Netherlands between 1610 and 1740. Place of study and graduation could not be identified Inhibitors,research,lifescience,medical in about a quarter of the group, and a further dozen were licensed to practice without medical degrees. Thus, about 40 Dutch Jews could be safely identified as having graduated from the local medical schools

during this period, while a further 24 Inhibitors,research,lifescience,medical Jews came to universities in the Netherlands to qualify as physicians. CONCLUSION In the eighteenth century the possibilities for Jews wishing to study medicine began to increase. Jews began to be admitted to the German medical schools from about 1720, and the first Jewish graduate in Scotland received his degree in 1739. Consequently the narrative of Jewish medical students changes dramatically.30 The story of Jewish medical Inhibitors,research,lifescience,medical students for many centuries was centered in Padua. While it attracted Jewish students from Germany and Poland, the numbers were small compared to those who were drawn from the territories under Venetian control. By the end of the seventeenth

century the Dutch medical schools began to challenge this ascendancy, given their geographical proximity to the centers of Jewish population and the quality of their medical teaching Inhibitors,research,lifescience,medical and scientific development, and provided the preferred place for Ashkenazi Jewish Inhibitors,research,lifescience,medical students. This continued until opportunities grew in other European countries during the eighteenth century enabling Jewish students to study medicine in their home communities. Footnotes Conflict of interest: No potential conflict of interest relevant to this article was reported.
Alzheimer’s disease (AD), the most prevalent neurodegenerative find more disorder, stems from a dual digestion of the amyloid precursor Casein kinase 1 protein (APP) by two proteases, β and γ secretases, which release the Aβ family of aggregation-prone peptides (collectively referred to as “Aβ”). Due to its hydrophobic nature, Aβ rapidly forms aggregates of various sizes.6 Small Aβ aggregative structures (also known as “oligomers”) have been shown to be the most toxic species and to correlate best with the development of AD which is characterized by neuronal loss, neuro-inflammation, cognitive failure, and eventually death.7,8 Hitherto, the mechanistic details of how Aβ oligomers lead to the manifestation of AD are poorly understood. Mutations that increase the production of Aβ have been shown to increase the risk to develop familial AD,9 and a mutation that reduces the Aβ production was found to be protective.