Alzheimer’s disease (AD) is the most common cause of dementia, typically showing progressive neurodegeneration in aging brains. The key signatures of the AD progression are the deposition of amyloid-beta (Aβ) peptides, the formation of tau tangles, and the induction of detrimental neuroinflammation leading to neuronal loss. However, conventional pharmacotherapeutic options are merely relying on the alleviation of symptoms that are limited to mild to moderate AD patients. Moreover, some of these medicines discontinued to use due to either the insignificant effectiveness in improving the cognitive impairment or the adverse side effects worsening essential bodily functions. One of the reasons for the failure is the lack of knowledge on the underlying mechanisms that can accurately explain the major causes of the AD progression correlating to the severity of AD. Therefore, there is an urgent need for the better understanding of AD pathogenesis and the development of the disease-modifying treatments, particularly for severe and late-onset AD, which have not been covered thoroughly. Here, we review the underlying mechanisms of AD progression, which have been employed for the currently established therapeutic strategies. We believe this will further spur the discovery of a novel disease-modifying treatment for mild to severe, as well as early- to late-onset, AD.

The evolution of preclinical in vitro cancer models has led to the emergence of human cancer-on-chip or microphysiological analysis platforms (MAPs). Although it has numerous advantages compared to other models, cancer-on-chip technology still faces several challenges such as the complexity of the tumor microenvironment and integrating multiple organs to be widely accepted in cancer research and therapeutics. In this review, we highlight the advancements in cancer-on-chip technology in recapitulating the vital biological features of various cancer types and their applications in life sciences and high-throughput drug screening. We present advances in reconstituting the tumor microenvironment and modeling cancer stages in breast, brain, and other types of cancer. We also discuss the relevance of MAPs in cancer modeling and precision medicine such as effect of flow on cancer growth and the short culture period compared to clinics. The advanced MAPs provide high-throughput platforms with integrated biosensors to monitor real-time cellular responses applied in drug development. We envision that the integrated cancer MAPs has a promising future with regard to cancer research, including cancer biology, drug discovery, and personalized medicine.

Background: Drug resistance has become a major concern for antiviral therapy in patients with chronic hepatitis B (CHB), leading to an increased risk of treatment failure. We aimed to identify the prevalence of hepatitis B virus (HBV) DNA polymerase mutations and to determine the frequency of HBV genotypes and subgenotypes in treatment-naive patients with CHB in Mekong Delta, Vietnam. Methods: Of the 550 drug-naive CHB patients from Mekong Delta, their serum samples were analyzed for HBV DNA mutations, genotypes, and subgenotypes using polymerase chain reaction sequencing. Results: Of the 550 patients who were infected with either HBV genotype B (72.9%) or genotype C (27.1%), the frequencies of subgenotypes were 19% B1, 3.6% B2, 10.3% B3, 39.8% B4, 0.4% C1, and 26.9% C2. The only mutation that was detected in 54 patients (10.7%) was rtV207M. The rtV207M mutation was found among 13.9% (51/368) of genotype B and among 2.2% (3/137) of genotype C (P < 0.0001). Discussion: Genotype B and subgenotype B4 are predominant in Mekong Delta. Only 1 mutation rtV207M is discovered in our study. These findings suggest that it is unnecessary to test for HBV resistance mutation before delivering antiviral therapy.