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Boehme et al (1971) reported a family (named Parry) in which 11 individuals over 4 generations were affected with adult-onset neuronal ceroid lipofuscinosis (NCL) in an autosomal dominant pattern of inheritance The strikingly consistent clinical picture was onset of a cerebellar syndrome at about age 31 years, followed by seizures, myoclonic jerks, and progressive dementia
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610951 - CEROID LIPOFUSCINOSIS, NEURONAL, 7; CLN7 Topcu et al (2004) reported the so-called Turkish variant of late-infantile CLN in 17 of 28 Turkish patients Most of the families were consanguineous The mean age at disease onset was 51 years (range, 2 to 7 years), with seizures or motor impairment as the most common presenting symptom
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A number sign (#) is used with this entry because neuronal ceroid lipofuscinosis-11 (CLN11) is caused by homozygous mutation in the GRN gene on chromosome 17qHeterozygous mutation in the GRN gene causes frontotemporal lobar degeneration with TDP43-inclusions () Description
Chieffo et al (1997) described the identification, cloning, and characterization of the human TBX1 gene, which maps to the center of the DiGeorge syndrome (DGS; 188400) chromosomal region on 22q112TBX1 is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box T-box genes are transcription factors involved in the regulation of .
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The article focuses upon the historic analysis of the process of national, cultural and linguistic homogenisation as a foundation of the social and political functioning of the nation state and the modern transnational European Union It ties the
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Spinocerebellar ataxia-21 (SCA21) is an autosomal dominant neurologic disorder characterized by onset in the first decades of life of slowly progressive cerebellar ataxia, which is associated with cognitive impairment in most patients (summary by Delplanque et al, 2014) For a general discussion of autosomal dominant spinocerebellar ataxia, see SCA1 ()
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