An increasing number of patients are visiting our hospital who have a chief complaint of neck and shoulder pain and/or headache but who do not have temporomandibular disorders (TMD). We carried out this study with a view to comparing the asymmetry of the facial skeleton or expression of such patients with those of healthy subjects. The incidence of such symptoms of patients and healthy subjects was examined by means of questionnaires. Asymmetry of the facial skeleton of patients was investigated by means of posterioanterior (PA) cephalograms. Facial asymmetry was analysed using the frontal view photographs of faces. We found that the patients had a higher incidence of various symptoms, including fatigability and irritability, in addition to neck and shoulder pain and headache, than the healthy subjects did. Both the healthy subjects and the patients had mandibular skeletal asymmetry to some degree, however, there was no significant difference between the two groups. On the other hand, the patients had a greater level of asymmetry of facial expression, chiefly of the lower face, than the healthy subjects did.
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http://dx.doi.org/10.1046/j.1365-2842.2001.00766.x | DOI Listing |
Background: Selecting the optimal dose for clinical development is especially problematic for drugs directed at CNS-specific targets. For drugs with a novel mechanism of action, these problems are often greater. We describe Xanamem's clinical pharmacology, including the approach to dose selection and proof-of-concept studies.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Merry Life Biomedical Company, Ltd., Tainan City, Taiwan, Taiwan.
Background: Alzheimer's disease (AD) is complex in pathogenesis and related to aging biology, especially in late-onset AD. We identified a novel synthetic curcumin analog TML-6 through the platform of 6 biomarkers of anti-aging, anti-inflammation, and anti-Aβ as the potential AD drug candidate. TML-6 exhibits multi-target effects on AD pathogenesis, including the activation of NrF-2, the regulation of autophagic machinery through mTOR, the inhibition of APP synthesis and reduction of Aβ, the upregulation of ApoE, and the inhibition of microglial activation.
View Article and Find Full Text PDFBackground: Progranulin (PGRN), a glycoprotein secreted by microglia and neurons, regulates lysosomal function, neuroinflammation, and has neurotrophic effects. Variants in the granulin gene (GRN) that cause a reduction of PGRN in plasma and cerebrospinal fluid (CSF) are associated with an increased risk of Alzheimer's disease (AD). The sortilin receptor (SORT1) on neurons and microglia regulates PGRN degradation.
View Article and Find Full Text PDFBackground: Microglial activation is one of the neuropathological hallmarks of Alzheimer's disease (AD). Evidence suggest that chronic activation of microglia cause neuroinflammation and neuronal injuries, contributing to cognitive impairment. Therefore, modulation of microglial pathway like CSF-1R represents an attractive therapeutic strategy.
View Article and Find Full Text PDFAmyloid β (Aβ) has been confirmed as a therapeutic target in AD by recent findings in Phase 3 trials with anti-Aβ antibodies. Modulators of γ-secretase (GSMs) are an emerging complementary approach to target amyloid. GSMs "modulate" the interaction between γ-secretase and amyloid precursor protein (APP), leading to a reduced production of long, amyloidogenic Aβ42 and Aβ40 and to concomitantly increased levels of the shorter, non amyloidogenic Aβ37 and Aβ38.
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