ライフサイエンスコーパス: Pick's disease

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1 inding repeat, detected other tau lesions in Pick's disease.

2 tations were identified in separate cases of Pick's disease.

3 gene in 30 cases of pathologically confirmed Pick's disease.

4 neuropathological studies on a patient with Pick's disease.

5 chromosome 17 (FTDP-17), historically termed Pick's disease.

6 instability successfully classified PSP from Pick's disease.

7 ith pathological tau protein accumulation in Pick's disease.

8 y heterogeneous; while pathologically proven Pick's disease and corticobasal degeneration were clinic

9 tients with other lobar dementias, including Pick's disease and corticobasal degeneration, by the abs

10 mutation and 3-repeat isoforms in brains of Pick's disease and familial tauopathy due to G272V tau m

11 nts in 149 patients and 50 controls from the PIck's disease and Progressive supranuclear palsy Preval

12 ive diseases-progressive supranuclear palsy, Pick's disease, and corticobasal degeneration-illustrate

13 Pick body-positive Pick's disease appeared three times.

14 The filaments of Pick's disease are loosely arranged in pathognomonic sph

15 eration, progressive supranuclear palsy, and Pick's disease, as well as by hereditary frontotemporal

16 The original diagnosis had been of Pick's disease based on frontotemporal atrophy, but re-e

17 l-insoluble gray and white matter regions of Pick's disease brains.

18 to analyze the tau isoform composition in 14 Pick's disease brains.

19 'tauopathies', which include Alzheimer's and Pick's diseases, but tau pathology is also found in the

20 stinct variety of hyperphosphorylated tau in Pick's disease compromises the long-term viability of se

21 er diagnoses in individual patients included Pick's disease, corticobasal degeneration and other tauo

22 s/nm length, but less dense than AD-PHFs and Pick's disease filaments.

23 osed as having Creutzfeldt-Jakob disease and Pick's disease in the absence of significant neocortical

24 isease (AD) differ from the tau filaments of Pick's disease in their morphology, distribution, and pa

25 utopsy demonstrated the classic pathology of Pick's disease, including massive neuron loss and gliosi

26 Therefore, Pick's disease is characterized by an accumulations of P

27 Pick's disease is characterized neuropathologically by d

28 Moreover, these data suggest that Pick's disease is not a separate entity but part of the

29 Pick's disease (n = 8) and multiple system atrophy (MSA,

30 ty of the autopsies in PPA have shown either Pick's disease or lobar atrophy without distinctive hist

31 of AD, corticobasal degeneration (CBD), and Pick's disease (PiD) brains by Western blots.

32 disease, frontotemporal lobar degeneration, Pick's disease, progressive supranuclear palsy and corti

33 lesions in three other tauopathies including Pick's disease, progressive supranuclear palsy and corti

34 number of other dementing disorders, such as Pick's disease, progressive supranuclear palsy, corticob

35 ); strongly asymmetric, distributed atrophy (Pick's disease); relatively symmetric, predominantly ext

36 , nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parki

37 om Family F had ballooned neurons typical of Pick's disease type B not found in Family D.

38 tau gene mutations are also associated with Pick's disease, we analyzed the tau gene in 30 cases of

39 tter define the spectrum of tau pathology in Pick's disease, we used biochemical, immunohistochemical

40 racterize and compare the filaments found in Pick's disease with those found in AD.

41 This is in contrast to Pick's disease without any tau gene mutations, which con

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