kwic
studies
studies
right
off
ON
148
1
100
500
strict
ELIZA cgi-bash version rev. 1.90
- Medical English LInking keywords finder for the PubMed Zipped Archive (ELIZA) -
return
kwic search for studies out of >500 occurrences
532339 occurrences (No.23 in the rank) during 5 years in the PubMed. [cache]
--- ABSTRACT ---
--- ABSTRACT END ---
[frequency of next (right) word to studies]
532339 occurrences (No.23 in the rank) during 5 years in the PubMed. [cache]
| 148) Large, prospective longitudinal studies are needed to clarify the association of Aβ with symptom development, progression, severity, and treatment response in LB disorders. |
| PMID:23831180 DOI:10.1016/j.jagp.2013.03.001 |
| 2015 The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry |
| * Amyloid PET Imaging in Lewy body disorders. |
| - Lewy body (LB) disorders, including Parkinson disease (PD), Parkinson disease dementia (PDD), and dementia with Lewy bodies (DLB), are the second most common type of neurodegenerative dementia. Although the pathological hallmarks of LB disorders are Lewy bodies and Lewy neurites, cortical amyloid-beta (Aβ) deposition is also often seen. The relationship between Aβ pathology and dementia in LB disorders is unclear. Recently, positron emission tomography Aβ ligands have been developed that enable in vivo imaging of Aβ. In this paper we review amyloid imaging studies in LB disorders. LB disorders are associated with lower mean cortical Aβ ligand binding compared with Alzheimer disease. In DLB and PDD many subjects have normal levels of cortical Aβ, though a subset show increased Aβ ligand binding. Those with DLB show greater ligand binding than PDD; binding does not appear to be increased in PD without dementia. Cortical Aβ deposition may be a factor in the development of cognitive impairment in some cases of dementia in LB disorders. Amyloid imaging is of limited use in the diagnosis of LB disorders but Aβ deposition may predict the future development of dementia in PD. Reports of correlation between Aβ deposition and symptom profile, severity, and progression have been inconsistent. Some results suggest a synergistic interaction between Aβ and α-synuclein. Interpretation of the current evidence is hampered by differing methodologies across studies and small sample sizes. Large, prospective longitudinal studies are needed to clarify the association of Aβ with symptom development, progression, severity, and treatment response in LB disorders. |
[
right
kwic]
(1)61  have |
(14)8 with |
(27)3 demonstrate |
(40)2 including |
| (2)47 *null* | (15)7 should |
(28)3 for |
(41)2 indicated |
| (3)32 of |
(16)6 is |
(29)3 however, |
(42)2 investigating |
| (4)26 are |
(17)6 we |
(30)3 performed |
(43)2 involving |
| (5)26 on |
(18)5 suggest |
(31)3 reported |
(44)2 it |
| (6)19 in |
(19)5 the |
(32)3 since |
(45)2 or |
| (7)17 were |
(20)4 as |
(33)3 which |
(46)2 provide |
| (8)16 and |
(21)4 demonstrated |
(34)2 about |
(47)2 published |
| (9)15 to |
(22)4 evaluating |
(35)2 also |
(48)2 regarding |
| (10)10 showed |
(23)4 from |
(36)2 can |
(49)2 targeting |
| (11)8 revealed |
(24)4 indicate |
(37)2 concerning |
(50)2 tested |
| (12)8 that |
(25)4 show |
(38)2 demonstrating |
(51)2 used |
| (13)8 using |
(26)3 based |
(39)2 has |
(52)2 was |
add keyword
--- WordNet output for studies ---