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Progranulin (GRN) and microtubule-associated protein tau (MAPT) mutations are associated with familial frontotemporal dementia, but recently some have also been found in clinically diagnosed AD cases [ 10, 11], and a recent study suggested that mutations in MAPT and GRN can be found in clinical AD with a frequency comparable to that of mutations in APP, PSEN1, and PSEN2 [ 7].
For example, deficits has been found in clinically presymptomatic familial autosomic dominant Alzheimer [10], or in clinically presymptomatic Huntington gene carriers individuals, who show deficits in motor control [11] [14], learning of motor sequences [15], and other non-motor functions, like memory and executive functions [16] [18], visuospatial processing [19] and olfaction [20].
Mutations in GRN and MAPT, two genes associated with frontotemporal dementia (FTD), have been found in clinically diagnosed AD cases.
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In the second season an additional 7 cases of pertussis were found in clinically unsuspected cases (7/257 = 2,7%).
No relation between ligament changes and time since injury (40 days to 59 years, median 5 years) was found in clinically referred WAD1-2 patients [ 23].
Infections caused by AIV of 8 HA subtypes, including H5 and H7, and 6 NA subtypes, were found in clinically healthy sentinel birds (Tables 1, 2).
In 91 joints (19%), signs of inflammation (effusion or synovitis) on ultrasonography were found in clinically uninflamed joints, whereas no ultrasonographic signs of inflammation were observed in 18 joints (4%) in which the clinicians described swelling and/or tenderness.
The true role of Campylobacter in canine gastroenteritis is uncertain as the bacteria may be found in clinically healthy dogs or often as a co-infection or intestinal carriage in diseased dogs.
In the study of Okuno et al only a subjective patient-reported amelioration of mucositis was reported but no reduction was found in clinically observed mucositis (Okuno et al, 1997).
This nucleus bearing at its 2-position a heterocycle through linker has been found in many clinically available antiulcer drugs.
Similar defects have been found in the ribosomopathies in humans, a clinically variable group of disorders which are associated with mutations in ribosome proteins and biogenesis factors (reviewed in [25], [26], [27]).
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