Seroprevalence of Lumpy Skin Disease and Livestock Owners' Knowledge, Attitudes and Practices in Selected Districts of Kazakhstan.

Genetic factors are known to underlie Early‐onset Parkinson's disease (EOPD), although data are mostly limited to monogenic cases. Multi‐genic (“oligogenic”) forms are rarely described and focus on coexisting single‐nucleotide (SNV) or exonic copy number variants (CNV) in PD‐associated genes typically detected by targeted multi‐gene panels. variants and the 22q11.2 microdeletion are known genetic risk factors for EOPD. Pathogenic changes convey a >10‐fold increased PD risk (mean age at onset (AAO): 50.7, SD 11.8 years). Certain variants confer an early AAO, and nearly half of pathogenic carriers present as EOPD. The recurrent 22q11.2 microdeletion is the most common pathogenic CNV in humans (~1 in 2148 live births) and accounts for ~0.4–0.5% of EOPD cases,, conferring a ~20‐70‐fold increased PD risk (mean AAO: 39.5, SD 8.5 years). Approximately >70% of affected individuals have EOPD, often with other neuropsychiatric features. We report a case of EOPD associated with both 22q11.2 microdeletion and severe pathogenic variant, and discuss potential implications. The patient is a 27‐year‐old, non‐Ashkenazi Jewish male diagnosed at age 14 with a de novo 22q11.2 microdeletion, later confirmed as a typical 2.5 Mb deletion. Lifetime history reflected neuropsychiatric and systemic features of 22q11.2 deletion syndrome (22q11.2DS; see Table ). At age 27, six years after limited antipsychotic exposure, he developed new‐onset right‐sided rest tremor, and examination revealed parkinsonism (Video ). Brain MRI and laboratory investigations were unremarkable. Dermal α‐synuclein seed amplification (SAA) assay was unrevealing (Table ). Levodopa/carbidopa (100/25 mg tid) resulted in symptom improvement (MDS‐UPDRS III score: 26 ➔17; Video ). However, subsequent development of motor and non‐motor fluctuation necessitated a switch to levodopa/carbidopa/entacapone therapy (Table ).