Oskar Fischer and the drusiform necrosis

The present days histopathologic signature of Alzheimer’s disease comprise ‘senile (neuritic) plaques’ (amyloid deposition, dystrophic axon terminals, activated microglia, and reactive astrocytes), and ‘neurofibrillary tangles’ found in presenile and senile cases.¹ These markers were identified in the beginning of the 20 century, as described below. Alois Alzheimer (1864-1915), a German psychiatrist and neuropathologist, described 1 case of ‘[pre] senile dementia’ (Senile Demenz), presented in 1906, and published as a short communication in 1907, with ‘remarkable changes of the neurofibrils’ (merkwürdige Veränderungen der Neurofibrillen) [neurofibrillary tangles] in brain cortical neurons, and mentioned briefly ‘miliary nodules’ (miliare Herdchen) [plaques], mostly abundant in the superficial brain cortical layers.² A brief time later, in 1910, Emil Kraepelin denominated this condition ‘Alzheimer’s disease’.³ Soon, Alzheimer presented a detailed description of plaques in a paper published in 1911, where he refers to these structures as Fischer’s plaques.⁴ Oskar Fischer (1876-1942), Czech psychiatrist and neuropathologist, examined 12 ‘senile dementia’ (Senile Demenz, Presbyophrenia) cases, where he noted foci of cortical ‘drusiform necrosis’ (later ‘multiple cerebral filamentous spheroids’) (drusige Nekrose [later Sphaerotrichia cerebri multiplex]) [neuritic plaques], the main focus of his studies at the time, described in a paper published in 1907.⁵ He confirmed these findings in a paper published in 1910 on 56 presenile and senile dementia cases. (Figure) He also described ‘coarse fibrillary proliferation of the ganglion cells’ (grobfaserige Fibrillenwucherung der Ganglienzellen) [neurofibrillary tangles], in a subset of 10 cases with plaques.⁶ Further studies clarified progressively the pathology of this kind of dementing condition. There is no doubt that Alzheimer deserves to be celebrated for his findings. However, Fischer should not be forgotten, considering that in present days, the plaques (neuritic plaques), which formation he described in great detail, are focus of the new therapeutic approaches for Alzheimer disease

Pathways and patterns of cell loss in verified Alzheimer's disease: a factor and cluster analysis of clinico-pathological subgroups

Thirty-seven patients with neuropathologicaUy verified Alzheimer's disease (AD) have been studied prospectively. A principal components analysis of neuron numbers in cortical and subcortical areas revealed two variables: Variable I with high loadings for the hippocampo-parahippocampo-parietal neuron counts and Variable n with high loadings for coeruleo-frontal cell numbers. Both may reflect functional neuroanatomical connections which may act as pathways of neurodegeneration in AD. A cluster analysis based on these neuron numbers yielded three groups of patients: Cluster A with low hippocampoparahippocampo-parietal cell counts, Cluster B with well-preserved neuron numbers, and Cluster C with low coeruleo-frontal neuron numbers. Differences in clinical features between these patient groups indicated the potential clinical relevance of these clusters

Incidence of psychoses by socio-economic areas in the city of Providence, Rhode Island, 1938 to 1948

Thesis (M.S.)--Boston University, 1949. This item was digitized by the Internet Archive

A study of the attitudes of the families of ten patients over sixty years of age requiring placement on trial visit from Boston State Hospital

Thesis (M.S.)--Boston Universit