This lack of a paternal force in the family enabled his growth and upbringing to be influenced mainly by his mother, a strong maternal personality, who guided his studies and encouraged his interest in medicine.

[3] The presentation of the case was received coldly and no questions were asked for clarification from the speaker, much less from the moderator of the debate, the psychiatrist Alfred Hoche, of Freudian origin and therefore an opponent of Kraepelin, who made Alzheimer’s report seem clinically and scientifically irrelevant.

[4] Alzheimer was convinced that he was facing a rare brain pathology and therefore decided to entrust the case to Perusini for a more in-depth and detailed evaluation of both the clinical aspects and the histopathological findings.

[7][1] The second part of his work contained an examination of the neurofibrillary alterations described by Alzheimer in 1908, Perusini reported that: "The altered neurofibrils in Bielschowsky solution have the most unusual aspects: wound in complex tangles which scarcely maintain the structure of nervous cells, they appear, within the tissue, almost as "skeletons'' of nervous cells …" In addition to the previously mentioned skeletons, other elements ought to be mentioned in which neurofibrils appear to be much thinner but arranged in complex convergent and divergent whirls' ' [1, p. 194].

Unfortunately, due to technical limitations on staining, Perusini was unable to draw precise conclusions regarding the correlation between senile plagues and neurofribillar alterations, and on the structure of neuroglia.

Perusini was raised in a patriotic family which likely influenced his decision to enlist, albeit hiding his professional identity, into the army as a volunteer at the outbreak of the First World War.

Eventually, the military discovered his medical professional background and was assigned to the first aid post in San Floriano del Collio, where on November 28, 1915 he was hit by shrapnel while assisting the wounded.

Although Peursini died at a young age of 36 and was thus unable to continue his research, his scientific contribution to the definition of the clinical and neuropathological aspects of neurodegenerative dementia, must be remembered.