Deep brain stimulation (DBS) is a surgical procedure that uses electrical neuromodulation to target specific regions of the brain, showing potential in the treatment of neurodegenerative disorders such as Parkinson’s disease (PD) and Alzheimer’s disease (AD). Despite similarities in disease pathology, DBS is currently only approved for use in PD patients, with limited literature on its effectiveness in AD. While DBS has shown promise in ameliorating brain circuits in PD, further research is needed to determine the optimal parameters for DBS and address any potential side effects. This review emphasizes the need for foundational and clinical research on DBS in different brain regions to treat AD and recommends the development of a classification system for adverse effects. Furthermore, this review suggests the use of either a low-frequency system (LFS) or high-frequency system (HFS) depending on the specific symptoms of the patient for both PD and AD.

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are two neurodegenerative diseases posing a significant disease burden due to their increasing prevalence and socio-economic cost. Traditional therapeutic approaches for these diseases exist but provide limited symptomatic relief without addressing the underlying pathologies. This review examines the potential of immunotherapy, specifically monoclonal antibodies (mAbs), as disease-modifying treatments for AD and PD. We analyze the pathological mechanisms of AD and PD, focusing on the roles of amyloid-beta (Aβ), tau (τ), and alpha-synuclein (α-syn) proteins. We discuss the latest advancements in mAb therapies targeting these proteins, evaluating their efficacy in clinical trials and preclinical studies. We also explore the challenges faced in translating these therapies from bench to bedside, including issues related to safety, specificity, and clinical trial design. Additionally, we highlight future directions for research, emphasizing the need for combination therapies, improved biomarkers, and personalized treatment strategies. This review aims to provide insights into the current state and future potential of antibody-based immunotherapy in modifying the course of AD and PD, ultimately improving patient outcomes and quality of life.

Background/Objectives: Colorectal cancer (CRC) and type 2 diabetes mellitus (T2DM) are two of the most rapidly rising chronic diseases globally. Despite appearing distinct, an emerging body of literature identifies shared etiopathogenic mechanisms mediated by gut microbiota. This review synthesizes 38 peer-reviewed studies to evaluate the compositional, metabolic, immune, and translational intersections of gut dysbiosis in the pathogenesis of T2DM-associated CRC. Methods: This narrative literature review examined 38 primary research articles (human and animal studies) retrieved from PubMed, Scopus, and Embase. Studies were selected based on relevance to the microbiota-mediated mechanisms linking T2DM and CRC, with a focus on compositional analysis, metabolomic shifts, immune activation, and therapeutic interventions. Results: The findings highlight a mechanistically rich overlap between T2DM and CRC through shared dysbiosis, characterized by depletion of SCFA-producing taxa (e.g., Faecalibacterium, Roseburia, Butyricicoccus), enrichment of pathobionts (e.g., Fusobacterium nucleatum, Peptostreptococcus), and the disruption of mucosal immunity and epithelial integrity. Metabolic shifts include reduced butyrate and increased toxic bile acids (e.g., deoxycholic acid), TMAO, and oxidative metabolites, while immune dysregulation features elevated LPS, IL-1β, CXCL3, and NF-κB signaling. Therapeutically, microbiota modulation via diet, metformin, and probiotics shows promise. Conclusions: Gut microbiota lies at the nexus of T2DM and CRC, functioning as a modifiable mediator rather than a passive bystander. Future research should prioritize longitudinal, multi-omic, and intervention-driven studies to enable personalized prevention and treatment strategies.

Alzheimer's Disease (AD) and Parkinson's Disease (PD) are two neurodegenerative diseases posing a significant disease burden due to their increasing prevalence and socio-economic cost. Traditional therapeutic approaches for these diseases exist but provide limited symptomatic relief without addressing the underlying pathologies. This review examines the potential of immunotherapy, specifically monoclonal antibodies (mAbs), as disease-modifying treatments for AD and PD. We analyze the pathological mechanisms of AD and PD, focusing on the roles of amyloid-beta (Aβ), tau (τ), and alpha-synuclein (α-syn) proteins. We discuss the latest advancements in mAbs therapies targeting these proteins, evaluating their efficacy in clinical trials and preclinical studies. We also explore the challenges faced in translating these therapies from bench to bedside, including issues related to safety, specificity, and clinical trial design. Additionally, we highlight future directions for research, emphasizing the need for combination therapies, improved biomarkers, and personalized treatment strategies. This review aims to provide insights into the current state and future potential of antibody-based immunotherapy in modifying the course of AD and PD, ultimately improving patient outcomes and quality of life.