path(HP:Neurodegeneration)

Entity

Name

Neurodegeneration

Namespace

hp

Namespace Version

releases/2019-02-12

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/c328ad964c08967a0417a887510b97b965a62fa5/external/hp-names.belns

TSubsequently, Wallerian degeneration and severe muscle wasting and motoric problems demon- strated the extensive neurodegeneration caused by the overexpression of human tau protein in a gene- dosage fashion. PubMed:12428809

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

In a yeast model expressing the N-terminal fragment of a polyQ-containing huntingtin protein, overexpression of the yeast HSP70 (SSA1) reduced aggregate formation, whereas the dominant-negative version of the fly homolog to HSPA1L, Hsc4-K71S, enhanced neurodegeneration (Warrick et al., 1999;) PubMed:27491084

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

For example, overexpression of the human TPR domain-containing co- chaperone CHIP suppresses neurodegeneration in fly models expressing polyQ-containing versions of ataxin 1 and the N-terminal huntingtin fragment (Al-Ramahi et al., 2006). PubMed:27491084

Degeneration of neurons in the brain of AD patients is associated with the activation of NF-B [7 PubMed:29179999

Elevated miRNA-146a in AD brain has been shown to also specifically target the interleukin-1 associated ki- nase-1 (IRAK-1) mRNAs, it is believed to contribute to altered innate immune responses and neuroinflammation in degenerating human brain cells and tissues in inflammatory neurodegenerative diseases including AD and in primary human brain cells stressed with ROS- generating metal sulfates [69]. PubMed:27288790

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

Degeneration of neurons in the brain of AD patients is associated with the activation of NF-B [7 PubMed:29179999