Objective: We systematically review the molecular mechanism of the interaction between lung cancer (LC) and tuberculosis (TB), and put forward the existing problems in order to provide suggestions for early intervention and future research direction.
Background: TB and LC are two global public health problems affecting human health. LC is the main cause of cancer-related death worldwide and TB is one of the leading causes of death among infectious diseases, especially in resource-poor areas. Previous studies have suggested that a history of TB may be associated with an increased risk of LC. With the improvement of LC treatment, the occurrence of pulmonary tuberculosis in the course of LC treatment is also frequently reported recently.
Methods: The molecular immunological mechanisms of interaction between LC and TB, and related epidemiological literature are reviewed. The research progress and problems to be solved are summarized.
Conclusions: Chronic inflammation, immune abnormalities, scar formation, gene mutations and drug effects caused by TB may be associated with the occurrence of LC induced by abnormalities in various molecular pathways. LC and decreased immunity during treatment may also increase the risk of latent TB activation or new TB infection through immune pathways. Data on dual burden areas of TB and LC are still lacking, and more clinical studies are needed to elucidate the association.
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http://dx.doi.org/10.21037/tlcr-21-465 | DOI Listing |
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the formation of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) composed of tau aggregates. Research in animal models has generated hypotheses on the underlying mechanisms of the interaction between Aβ and tau pathology. In support of this interaction, results from clinical trials have shown that treatment with anti-Aβ monoclonal antibodies (mAbs) affects tau pathology.
View Article and Find Full Text PDFBackground: The therapeutic management of dementia with Lewy bodies (LBD) is a challenge given the high sensitivity to drugs in this disease. This is particularly sensitive with regard to the management of parkinsonism. In particular, treatment of motor symptoms with levodopa or dopaminergic agonists poses a risk of worsening cognitive and behavioral symptoms.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The University of Texas Health Science Center at Houston, Houston, TX, USA.
Background: Developing drugs for treating Alzheimer's disease (AD) has been extremely challenging and costly due to limited knowledge on underlying biological mechanisms and therapeutic targets. Repurposing drugs or their combination has shown potential in accelerating drug development due to the reduced drug toxicity while targeting multiple pathologies.
Method: To address the challenge in AD drug development, we developed a multi-task machine learning pipeline to integrate a comprehensive knowledge graph on biological/pharmacological interactions and multi-level evidence on drug efficacy, to identify repurposable drugs and their combination candidates RESULT: Using the drug embedding from the heterogeneous graph representation model, we ranked drug candidates based on evidence from post-treatment transcriptomic patterns, mechanistic efficacy in preclinical models, population-based treatment effect, and Phase 2/3 clinical trials.
Alzheimers Dement
December 2024
Edith Cowan University, Perth, Western Australia, Australia.
Background: Accumulation of amyloid beta 42 (Aβ42) senile plaques is the most critical event leading to Alzheimer's disease (AD). Currently approved drugs for AD have not been able to effectively modify the disease. This has caused increasing research interests in health beneficial nutritious plant foods as viable alternative therapy to prevent or manage AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
ADEL Institute of Science & Technology (AIST), ADEL, Inc., Seoul, Korea, Republic of (South).
Background: The spatiotemporal pattern of the spread of pathologically modified tau through brain regions in Alzheimer's disease (AD) can be explained by prion-like cell-to-cell seeding and propagation of misfolded tau aggregates. Hence, to develop targeted therapeutic antibodies, it is important to identify the seeding- and propagation-competent tau species. The hexapeptide VQIINK of tau is a critical region for tau aggregation, and K280 is acetylated in various tauopathies including AD.
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