| Alfons Maria Jakob | |
| Birth Place: | Aschaffenburg, Kingdom of Bavaria, German Empire |
| Death Place: | Hamburg, Weimar Republic |
| Nationality: | German |
| Field: | Neurology |
| Known For: | Neuropathology |
Alfons Maria Jakob (2 July 1884 - 17 October 1931) was a German neurologist who worked in the field of neuropathology.
He was born in Aschaffenburg, Bavaria and educated in medicine at the universities of Munich, Berlin, and Strasbourg, where he received his doctorate in 1908. During the following year, he began clinical work under the psychiatrist Emil Kraepelin and did laboratory work with Franz Nissl and Alois Alzheimer in Munich.[1]
In 1911, by way of an invitation from Wilhelm Weygandt,[2] he relocated to Hamburg, where he worked with Theodor Kaes and eventually became head of the laboratory of anatomical pathology at the psychiatric State Hospital Hamburg-Friedrichsberg. Following the death of Kaes in 1913, Jakob succeeded him as prosector.[1] During World War I he served as an army physician in Belgium,[2] and afterwards returned to Hamburg. In 1919, he obtained his habilitation for neurology and in 1924 became a professor of neurology. Under Jakob's guidance the department grew rapidly. He made significant contributions to knowledge on concussion and secondary nerve degeneration and became a doyen of neuropathology.[3]
Jakob was the author of five monographs and nearly 80 scientific papers.[2] His neuropathological research contributed greatly to the delineation of several diseases, including multiple sclerosis and Friedreich's ataxia. He first recognised and described Alper's disease and Creutzfeldt–Jakob disease (named along with Munich neuropathologist Hans Gerhard Creutzfeldt).[1] He gained experience in neurosyphilis, having a 200-bed ward devoted entirely to that disorder. Jakob made a lecture tour of the United States (1924) and South America (1928), of which, he wrote a paper on the neuropathology of yellow fever.[2] [3]
He suffered from chronic osteomyelitis for the last seven years of his life. This eventually caused a retroperitoneal abscess and paralytic ileus from which he died following operation.[1]