Disease relevance of Pick Disease of the Brain

• In contrast to AD, NGF receptor-containing cortical neurons were not observed in Parkinson disease, Pick disease, or Shy-Drager syndrome [1].
• Comparative biochemistry of tau in progressive supranuclear palsy, corticobasal degeneration, FTDP-17 and Pick's disease [2].
• Therefore, Pick's disease is characterized by an accumulations of Pick bodies in the hippocampal region and cortex as well as the presence of three and four microtubule-binding repeat tau pathology in both cortical gray and white matter that distinguish this tauopathy from other neurodegenerative disorders [3].
• Pick's disease (n = 8) and multiple system atrophy (MSA, n = 15) [4].
• Neuropathologic examination indicated that among 30 patients with a clinical history of severe dementia, 22 had Braak and Braak stage V-VI Alzheimer disease, 3 had combined Alzheimer and Parkinson disease, 3 had Pick disease and 2 had severe hippocampal sclerosis [5].

Psychiatry related information on Pick Disease of the Brain

• These two subjects, both homozygous for the APOE-epsilon4 allele, were primarily diagnosed as having Creutzfeldt-Jakob disease and Pick's disease in the absence of significant neocortical amyloid deposition [6].
• In the temporal cortex, there was a smaller proportion of M1 receptors in atypical Pick's disease than in the controls or in the patients with Alzheimer's disease and dementia with Lewy bodies [7].
• Clinical diagnoses included probable Alzheimer disease (n = 5), possible Alzheimer disease (n = 1), Pick disease (n = 2), and primary progressive aphasia (n = 2) [8].
• Less frequent disorders are cortico-basal ganglionic degeneration (CBGD), frontotemporal dementia with chromosome 17 (FTDP-17), Pick's disease, parkinsonian-dementia complex of Guam, Pallidonigral degeneration, Wilson's disease and a rigid variant of Huntington's disease [9].

High impact information on Pick Disease of the Brain

• A novel presenilin 1 mutation associated with Pick's disease but not beta-amyloid plaques [10].
• Frontotemporal degeneration, Pick's disease, Pick complex, and Ravel [11].
• Sarkosyl-insoluble tau extracted from the cerebral cortex showed the presence of straight and twisted tau filaments and a pattern of pathological tau bands similar to that of Pick's disease [12].
• Results showed significant increases in chlorine, iron, manganese, sodium, and phosphorus and significant decreases in chromium, cesium, rubidium, and selenium and in the mean freeze-dried to wet-weight ratio for patients with Pick's disease compared with control patients [13].
• By this assay and subsequent co-immunoprecipitation and glutathione S-transferase pull-down assays, we discovered and confirmed that Saitohin interacts with peroxiredoxin 6, a unique member of that family that is bifunctional and the levels of which increase in Pick disease [14].

Chemical compound and disease context of Pick Disease of the Brain

• With the exception of rare immunoreactive Pick bodies in one case of Pick's disease, no other structure was recognized by HNE pyrrole adduct antiserum in this series of patients [15].
• Alterations of muscarinic acetylcholine receptors in atypical Pick's disease without Pick bodies [7].
• A 61-year-old man with presumed Pick's disease was successfully treated with fluoxetine for pathological affect [16].
• Sections of formaldehyde-fixed paraffin-embedded cortical and hippocampal brain tissue from five cases with senile dementia of Alzheimer type (SDAT) and five cases with Pick's disease (PD) were immunostained with the monoclonal antibodies (mabs) 147, RT 97, BF 10 and 8D8 with and without pretreatment with alkaline phosphatase (AP) or trypsin (Tr) [17].
• The water-soluble proteins of the cerebral gray matter and some enzyme systems (cholinesterase, acetylcholinesterase, lactate dehydrogenase, malate dehydrogenase, acid phosphatase) were studied in 9 autopsy cases of Alzheimer's presenile or senile dementia, 1 case of Pick's disease and 1 case of cerebral arteriosclerosis [18].

Biological context of Pick Disease of the Brain

• BACKGROUND: Clinical Pick's disease, or FTD with parkinsonism, has been described in several families linked to chromosome 17 (FTDP-17) [19].
• The p38 pathway is activated in Pick disease and progressive supranuclear palsy: a mechanistic link between mitogenic pathways, oxidative stress, and tau [20].
• Active stress kinase p38 enhances and perpetuates abnormal tau phosphorylation and deposition in Pick's disease [21].

Anatomical context of Pick Disease of the Brain

• The filaments of Pick's disease are loosely arranged in pathognomonic spherical inclusions found in ballooned neurons, whereas the tau pathology of AD is classically described as a triad of neuropil threads, neurofibrillary tangles, and dystrophic neurites surrounding and invading plaques [22].
• In contrast to classic Pick's disease, there were no Pick bodies in the hippocampus [23].
• Abnormal accumulation of proteins in filamentous cytoplasmic inclusions is a hallmark of several neurodegenerative disorders, including Alzheimer disease (AD) and Pick disease (PD) [24].
• The typical lesions of corticobasal degeneration and Pick's disease were revealed by immunohistochemistry, including the presence of Pick bodies and achromatic swollen neurons, neuritic alterations, and neurofibrillary tangles [25].
• In DNTC, the degree and distribution of the basal ganglia lesions, except for nigral lesions, were analogous to those found in Pick's disease with Pick bodies [26].

Gene context of Pick Disease of the Brain

• Furthermore, the apolipoprotein epsilon4 allele (APOE epsilon4) may be associated with Pick disease [27].
• In contrast, TPPP/p25 is not associated with abnormally phosphorylated tau in various inclusions of Pick's disease (PiD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD) [28].
• We examined p25 immunoreactivity in brains from sporadic and familial AD cases, as well as other neurologic diseases that exhibit NFT, such as Down's syndrome (DS), Pick's disease (Pick), corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), frontotemporal dementia (FTD) [29].
• Dyrk1 phosphorylates the human microtubule-associated protein tau at Thr212 in vitro, a residue that is phosphorylated in fetal tau and hyper-phosphorylated in Alzheimer disease (AD) and tauopathies, including Pick disease (PiD) [30].
• These results are of interest since overexpression of clusterin is also observed in other neuro-degenerative diseases such as Alzheimer's and Pick's disease [31].

Analytical, diagnostic and therapeutic context of Pick Disease of the Brain

• OBJECTIVES: To define the cognitive characteristics of Pick disease (PcD), and to determine which features distinguish PcD from Alzheimer disease (AD), in a cross-sectional and longitudinal study [32].
• Here, PDHc and SDH activity were stimulated with each of the two stereoisomers of alpha lipoic acid in post-mortem parietal brain cortex of patients with DAT, DVT, and one case of Pick's disease and compared to stimulation effects in a control group, matched for age, sex, post-mortem delay, and storage time of brain tissue [33].

References