Magic™ Anti-Tau (Phospho S404) monoclonal antibody, clone FQS3716

Hemangiomas most commonly occur in the skin or mucosa and are rare in skeletal muscle. There have been almost no reports of their development in skeletal muscle of the head and neck region. A case of cavernous hemangioma of the temporalis muscle is reported along with a short discussion of the literature. A 69-year-old woman presented to our department with a chief complaint of swelling in the left temporal region. She had noticed a painless mass in this region around six months earlier and had consulted a local dental clinic, which had referred her to our department for further investigation and treatment. On general physical examination, she was of moderate build and well nourished. External oral examination showed a palpable, elastic-soft, semispherical mass in the left temporal region measuring 37 mm x 36 mm. Internal oral examination showed nothing of note. A clearly demarcated hyperintensity between the left temporalis muscle and the left temporalis fascia was visible on T2-weighted and short tau inversion recovery (STIR) magnetic resonance imaging (MRI), and this was clinically diagnosed as a tumor of the left temporal region. Thus, tumor enucleation of the left temporal region was scheduled and performed under general anesthesia. The histopathological diagnosis was cavernous hemangioma. The patient's postoperative course has been good, with no recurrence nine months after surgery.

Alpha-synuclein is the main protein component of Lewy bodies, the pathological hallmark of Parkinson's disease. However, genetic modifiers of cerebrospinal fluid (CSF) alpha-synuclein levels remain unknown. The use of CSF levels of amyloid beta(1-42), total tau, and phosphorylated tau(181) as quantitative traits in genetic studies have provided novel insights into Alzheimer's disease pathophysiology. A systematic study of the genomic architecture of CSF biomarkers in Parkinson's disease has not yet been conducted. Here, genome-wide association studies of CSF biomarker levels in a cohort of individuals with Parkinson's disease and controls (N = 1960) were performed. PD cases exhibited significantly lower CSF biomarker levels compared to controls. A SNP, proxy for APOE epsilon 4, was associated with CSF amyloid beta(1-42) levels (effect = - 0.5, p = 9.2 x 10(-19)). No genome-wide loci associated with CSF alpha-synuclein, total tau, or phosphorylated tau(181) levels were identified in PD cohorts. Polygenic risk score constructed using the latest Parkinson's disease risk meta-analysis were associated with Parkinson's disease status (p = 0.035) and the genomic architecture of CSF amyloid beta(1-42) (R-2 = 2.29%; p = 2.5 x 10(-11)). Individuals with higher polygenic risk scores for PD risk presented with lower CSF amyloid beta(1-42) levels (p = 7.3 x 10(-04)). Two-sample Mendelian Randomization revealed that CSF amyloid beta(1-42) plays a role in Parkinson's disease (p = 1.4 x 10(-05)) and age at onset (p = 7.6 x 10(-06)), an effect mainly mediated by variants in the APOE locus. In a subset of PD samples, the APOE epsilon 4 allele was associated with significantly lower levels of CSF amyloid beta(1-42) (p = 3.8 x 10(-06)), higher mean cortical binding potentials (p = 5.8 x 10(-08)), and higher Braak amyloid beta score (p = 4.4 x 10(-04)). Together these results from high-throughput and hypothesis-free approaches converge on a genetic link between Parkinson's disease, CSF amyloid beta(1-42), and APOE.