Over the last decades, our knowledge of the key pathogenic mechanisms of Alzheimer's disease (AD) has dramatically improved. Regarding the limitation of current therapeutic strategies for the treatment of multifactorial diseases, such as AD, to be translated into the clinic, there is a growing trend in research to identify risk factors associated with the onset and progression of AD. Here, we review the current literature with a focus on the relationship between gastrointestinal (GI)/liver diseases during the lifespan and the incidence of AD, and discuss the possible mechanisms underlying the link between the diseases. We also aim to review studies evaluating the possible link between the chronic use of the most common GI medications and the future risk of AD development.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.lfs.2021.120088 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Review of Associations of Diabetes and Insulin Resistance With Brain Health in Three Harmonised Cohort Studies of Ageing and Dementia.
Diabetes Metab Res Rev
January 2025
Rush Alzheimer's Disease Centre, Rush University Medical Center, Chicago, Illinois, USA.
Diabetes increases the risk of dementia, and insulin resistance (IR) has emerged as a potential unifying feature. Here, we review published findings over the past 2 decades on the relation of diabetes and IR to brain health, including those related to cognition and neuropathology, in the Religious Orders Study, the Rush Memory and Aging Project, and the Minority Aging Research Study (ROS/MAP/MARS), three harmonised cohort studies of ageing and dementia at the Rush Alzheimer's Disease Center (RADC). A wide range of participant data, including information on medical conditions such as diabetes and neuropsychological tests, as well as other clinical and laboratory-based data collected annually.
View Article and Find Full Text PDFSubventricular Accumulation of Cu in the Aging Mouse Brain Does Not Associate with Anticipated Increases in Markers of Oxidative Stress.
ACS Chem Neurosci
January 2025
School of Molecular and Life Sciences, Faculty of Science and Engineering, Curtin University, Bentley, WA 6845, Australia.
Natural aging is associated with mild memory loss and cognitive decline, and age is the greatest risk factor for neurodegenerative diseases, such as Alzheimer's disease. There is substantial evidence that oxidative stress is a major contributor to both natural aging and neurodegenerative disease, and coincidently, levels of redox active metals such as Fe and Cu are known to be elevated later in life. Recently, a pronounced age-related increase in Cu content has been reported to occur in mice and rats around a vital regulatory brain region, the subventricular zone of lateral ventricles.
View Article and Find Full Text PDFLoss of dental pulp potentially increased the risk of Alzheimer's dementia.
J Dent Sci
January 2025
Department of Oral Physiology, School of Dentistry, Seoul National University, Seoul, Republic of Korea.
Background/purpose: Chronic periodontitis and tooth loss contribute to cognitive decline. Since many biological processes are shared by loss of teeth and loss of pulps, this study investigated the potential association between loss of pulp and the development of dementia.
Materials And Methods: A retrospective cohort analysis was conducted to investigate the association between dental treatment and the development of dementia.
Low-dose intranasal deferoxamine modulates memory, neuroinflammation, and the neuronal transcriptome in the streptozotocin rodent model of Alzheimer's disease.
Front Neurosci
January 2025
HealthPartners Institute, Neuroscience Research, HealthPartners Neuroscience Center, Saint Paul, MN, United States.
Introduction: Intranasal (IN) deferoxamine (DFO) has emerged over the past decade as a promising therapeutic in preclinical experiments across neurodegenerative and neurovascular diseases. As an antioxidant iron chelator, its mechanisms are multimodal, involving the binding of brain iron and the consequent engagement of several pathways to counter pathogenesis across multiple diseases. We and other research groups have shown that IN DFO rescues cognitive impairment in several rodent models of Alzheimer Disease (AD).
View Article and Find Full Text PDFNeuroinflammation mediates the progression of neonate hypoxia-ischemia brain damage to Alzheimer's disease: a bioinformatics and experimental study.
Front Aging Neurosci
January 2025
School of Medicine, Yunnan University, Kunming, China.
Background: Traumatic brain injury (TBI) can generally be divided into focal damage and diffuse damage, and neonate Hypoxia-Ischemia Brain Damage (nHIBD) is one of the causes of diffuse damage. Patients with nHIBD are at an increased risk of developing Alzheimer's disease (AD). However, the shared pathogenesis of patients affected with both neurological disorders has not been fully elucidated.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!