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Pick’s disease, also known as Pick disease and PiD, is a rare neurodegenerative disease. While the term Pick’s disease was once used to represent a specific group of clinical syndromes with symptoms attributable to frontal and temporal lobe dysfunction, it is now used (at least among professionals in the field) to mean a specific pathology that is just one of the causes of the clinical syndrome now known as frontotemporal lobar degeneration. Some people still use the term Pick’s disease to mean the more general clinical syndrome of frontotemporal lobar degeneration, but this has previously led to confusion among both professionals and patients and so its use should be restricted to the specific pathological subtype described below.
Pick’s disease (the pathology) causes progressive destruction of nerve cells in the brain and causes tau proteins to accumulate into “Pick bodies”[1] that are a defining characteristic of the disease.
Pick’s disease is named after Arnold Pick, a professor of psychiatry from the University of Prague who first discovered and described the disease in 1892 by examining the brain tissue of several deceased patients with histories of dementia.[2][1] As a result, the characteristic histological feature of this disease – a protein tangle that appears as a large body in neuronal tissue – is named a Pick body. In 1911, Alois Alzheimer also noted the complete absence of senile plaques and neurofilbrillary tangles as well as the presence of Pick Bodies and occasional ballooned neurons.[2]
Pick’s disease is one of the causes of the clinical syndrome of frontotemporal lobar degeneration which has three subtypes. Pick’s disease pathology is associated more with the frontotemporal dementia and progressive nonfluent aphasia subtypes than the semantic dementia subtype.
Whilst other pathologies causing frontotemporal lobar degeneration are associated with a genetic cause, there is no evidence in the modern literature that classical Pick’s disease pathology can run in families or has a genetic cause.
PiD was first recognized as a distinct disease separate from other neurodegenerative diseases because of the presence of large, dark-staining aggregates of proteins in neurological tissue as well as the aforementioned ballooned cells, which are known as Pick cells. Pick bodies are almost universally present in patients with PiD, but some new cases of atypical Pick’s disease have come to light that lack noticeable Pick bodies.[3] A variety of stains can aid in the visualization of Pick bodies and Pick cells, but immunohistochemical staining using anti-tau and anti-ubiquitin antibodies have proven the most efficient and specific.[4] Hematoxylin and eosin staining allows visualization of another population of Pick cells, which are both tau and ubiquitin protein negative. Several different silver impregnation stains have been used, including the Bielschowsky, Bodian, and Gallyas methods.[5][3] The latter two techniques are sensitive enough to allow PiD to be distinguished from Alzheimer’s disease as the Bodian will bind preferentially to cells with PiD as compared to the Gallyas method, which preferentially binds to the cells with Alzheimer’s.[5]
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