We recently reported a correlation between proteolytic product of gelsolin (carboxyl-terminal fragment of gelsolin, gelsolin-CTF) and severity of Alzheimer's disease.
The amyloid-β (Aβ) peptide is contained within the C-terminal fragment (β-CTF) of the amyloid precursor protein (APP) and is intimately linked to Alzheimer's disease.
In this review, we summarize observations indicating that both CTF and Abeta may participate in the neuronal degeneration in the progress of AD by differential mechanisms.
Intriguingly, Alzheimer's disease (AD)-associated pathological proteins, such as BACE-1, APP, β-CTF, α-CTF, Aβ <sub>1-42</sub> and phosphorylated tau proteins (S199, S396, T205, S214 and S404), were substantially increased after BPA exposure, and these effects were abrogated by insulin and rosiglitazone treatment; these findings underscore the specific roles of insulin signaling in BPA-mediated AD-like neurotoxicity.
Here we report that NRBF2 (nuclear receptor binding factor 2), a key component and regulator of the PtdIns3K, is involved in APP-CTFs homeostasis in AD cell models.
The AAV1-I(2NTF-CTF) rats not only offer a disease-relevant model of the sporadic form of Alzheimer's disease but also represent a practical and widely available animal model.
AβPP-CTF, Aβ45, and aggregated Aβ colocalized most strongly with mitochondria and endosomes and less with lysosomes and autophagosomes.Differences in iAβ by sex were minor.
CADM1 α-shedding was induced in AS and DN kidneys and derived from the decrease in full-length CADM1 (FL-CADM1) and increase of the COOH-terminal fragment (α-CTF).
A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX (P<sub>best</sub>=5.8 × 10<sup>-10</sup>), and supported three regions previously implicated in BD susceptibility: MAD1L1 (P<sub>best</sub>=1.9 × 10<sup>-9</sup>), TRANK1 (P<sub>best</sub>=2.1 × 10<sup>-9</sup>) and ODZ4 (P<sub>best</sub>=3.3 × 10<sup>-9</sup>).