AD: Shocked! The peak value of plasma Aβ42/Aβ40 began to decline 41 years before the deposition of brain Aβ! Alzheimer's diseases: New discovery on plasma Aβ42/Aβ40. AD: Shocked! The peak value of plasma Aβ42/Aβ40 began to decline 41 years before the deposition of brain Aβ! Amyloid β (Aβ) plaque deposition and phosphorylated tau (p-tau) protein tangles are two important pathological features of Alzheimer's disease (AD), and there are many kinds of AD biomarkers derived around them, Knowledge of the longitudinal trajectories of key markers could not only help improve the selection and monitoring of participants in clinical trials, but also help identify those at high risk for neurodegenerative changes and cognitive impairment. Although research on AD biomarkers has increased substantially in recent years, research on longitudinal changes in biomarkers is relatively limited. Studies have shown that the levels of plasma Aβ 42 /Aβ 40 , p-tau181 and glial fibrillary acidic...
bioRxiv: Scientists have identified a new potential target for the treatment of lung cancer In cancer research, personalized medicine therapy often uses special genetic changes in a single tumor to find its weakness and attack it. Many tumors carry high levels of mutations, perhaps because of a special antiviral defense Mechanism-APOBEC system, which can accidentally damage DNA and induce mutations. The analysis of cancer mutation characteristics often provides researchers with a large amount of information on the source of mutations, and can guide the use of clinical therapies, including immunotherapy, etc.; in particular, APOBEC3A (A3A, apolipoprotein B mRNA editing enzyme catalyzed polypeptide-like protein 3A, apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3A) has now become the main driver of mutations in cancer cells. Its expression can cause DNA damage and become sensitive to ATR and CHK1 checkpoint kinase inhibitor therapy. Image source: https://www.biorxiv.org/...
