Prof.Jong-LingFuh - AOCE 2026

Dr. Jong-Ling Fuh is Vice Director of the Department of Neurology at Taipei Veterans General Hospital and Professor of Neurology at National Yang Ming Chiao Tung University. She earned her medical degree from National Yang-Ming University and completed a fellowship in Behavioral Neurology at UCLA. A certified Diplomat of the Taiwan Board of Neurology, she has served as an attending neurologist and educator since 2007. Dr. Fuh is deeply engaged in academic leadership, serving on the board of the Asian Society Against Dementia Congress and holding deputy direcotr-in-chief roles with the Journal of the Chinese Medical Association. She is a Fellow of the American Academy of Neurology and currently Executive Director of the Taiwan Dementia Society, where she previously served as President. Her contributions to clinical education and research have earned widespread recognition. She was named among Stanford University’s Top 2% Scientists (2020–2025) and received Outstanding Clinical Teaching Awards (2017, 2021) and Outstanding Physician Awards (2010, 2015) from Taiwan’s Veterans Affairs Commission. Her research accolades include First Place Poster Award at the 2021 VGH–UST Joint Research Program, Best Poster at the 2008 Asian Dementia Congress, and the Millennium Best Essay Award (2000). Dr. Fuh’s research focuses on dementia epidemiology and biomarkers in Alzheimer’s and Parkinson’s disease with dementia. She has authored over 400 peer-reviewed publications, advancing the field of neuropsychology and dementia care.

22 MARCH

Time	Session

11:00 12:30	[DAROC Symposium 4] Complication Diabetes Mellitus and Emerging Complications Diabetes and Heart Failure: A Dual Epidemic Kuo-Meng LiaoTaiwan Speaker Diabetes and Heart Failure: A Dual EpidemicDiabetes mellitus (DM) and heart failure (HF) are tightly interconnected disease states that interact through complex and bidirectional cardio-metabolic mechanisms. Among HF phenotypes, heart failure with preserved ejection fraction (HFpEF) shows the strongest association with DM, reflecting shared pathophysiological pathways beyond traditional ischemic heart disease. Epidemiologically, DM confers a two- to four-fold increased risk of incident HF, with a disproportionate burden of HFpEF. Patients with HFpEF exhibit a high prevalence of DM and insulin resistance, accompanied by worse exercise intolerance, higher hospitalization rates, and increased mortality. These observations support the concept that DM is not merely a comorbidity but a central contributor to HFpEF pathogenesis. Mechanistically, chronic hyperglycemia and insulin resistance initiate a cascade of systemic and myocardial abnormalities. Endothelial dysfunction, coronary microvascular inflammation, and impaired nitric oxide–cyclic GMP–protein kinase G signaling promote cardiomyocyte stiffness and diastolic dysfunction. Metabolic inflexibility, characterized by excessive fatty acid utilization and impaired glucose oxidation, reduces myocardial energetic efficiency. In parallel, advanced glycation end products, oxidative stress, mitochondrial dysfunction, and lipotoxicity drive myocardial fibrosis and adverse extracellular matrix remodeling. These myocardial changes are further amplified by extracardiac factors common in DM—obesity, chronic kidney disease, systemic inflammation, and autonomic imbalance—creating the multi-organ HFpEF syndrome. Conversely, HF exacerbates insulin resistance through neurohormonal activation, inflammation, and skeletal muscle hypoperfusion, reinforcing a vicious cycle between metabolic and cardiac dysfunction. Recognition of this cross-talk has important therapeutic implications, as exemplified by sodium–glucose cotransporter 2 inhibitors, which improve HF outcomes through mechanisms extending beyond glucose lowering. In summary, DM and HFpEF are linked through shared mechanistic pathways involving metabolism, microvascular dysfunction, and inflammation. A mechanistic understanding of this interaction is essential for developing integrated, phenotype-specific cardio-metabolic strategies. Metabolic Dysfunction and Brain Health: Diabetes as a Risk Factor for Dementia Jong-Ling FuhTaiwan Speaker Metabolic Dysfunction and Brain Health: Diabetes as a Risk Factor for DementiaType 2 Diabetes Mellitus (T2DM) is no longer confined to glucose dysregulation—it is a systemic accelerator of brain aging and a major modifiable risk factor for dementia. Epidemiologic and mechanistic studies reveal that poor glycemic control, including both hyper- and hypoglycemia, significantly increases dementia risk. Data from Taiwan’s National Health Insurance Database show that pronounced glycemic fluctuations more than double this risk, while meta-analyses identify prolonged diabetes duration, elevated HbA1c, hypertension, and insulin resistance as key predictors of cognitive decline. Pathophysiological evidence links chronic hyperglycemia and insulin resistance to neuroinflammation, oxidative stress, and tau pathology. Neuroimaging studies show hippocampal atrophy and white matter degradation in patients with poorly controlled diabetes. Cardiovascular comorbidities amplify this burden: diabetes combined with coronary artery disease doubles the risk of vascular dementia. Encouragingly, therapeutic innovation offers hope. Glucose-lowering agents such as GLP-1 Receptor Agonists (GLP-1RAs) and SGLT2 Inhibitors (SGLT2is) may extend their cardiometabolic benefits to the brain. GLP-1RAs have shown a 45% reduction in dementia risk in real-world and trial-based analyses, reinforcing the interconnectedness of metabolic, vascular, and neurodegenerative pathways. In East Asia, where diabetes and dementia are surging, the clinical imperative is clear: brain health must be a core outcome of metabolic care. Early glycemic optimization, vascular protection, and neuroprotective therapies may define the next frontier in dementia prevention. Sleep Apnea in Diabetes: A Silent Aggravator Li-Pang ChuangTaiwan Speaker Sleep Apnea in Diabetes: A Silent AggravatorObstructive sleep apnea (OSA) is a highly prevalent clinical disease affecting more than 10% of the adult population. It is characterized by repetitive episodes of partial or total upper airway obstruction during sleep, resulting in subsequent sleep fragmentation and intermittent hypoxia. Accumulating studies reveal that OSA is an independent risk factor for consequent cardiovascular morbidities, such as myocardial infarction, heart failure, nocturnal dysrhythmias and pulmonary hypertension. Currently, OSA can be treated by means of positive airway pressure therapy, pharmacological therapy and surgical intervention. OSA is a silent aggravator of diabetes because it worsens glucose metabolism and insulin resistance through mechanisms like intermittent hypoxia, sleep fragmentation, and sympathetic nervous system activation. This creates a bidirectional relationship where OSA increases the risk and severity of diabetes, and diabetes can worsen OSA. Treating OSA may improve glycemic control, and screening for it is crucial, especially in individuals with type 2 diabetes, particularly those who are obese. 3F Banquet Hall

Time

Session

11:00

12:30

[DAROC Symposium 4] Complication

Diabetes Mellitus and Emerging Complications

Diabetes and Heart Failure: A Dual Epidemic

Kuo-Meng LiaoTaiwan Speaker Diabetes and Heart Failure: A Dual EpidemicDiabetes mellitus (DM) and heart failure (HF) are tightly interconnected disease states that interact through complex and bidirectional cardio-metabolic mechanisms. Among HF phenotypes, heart failure with preserved ejection fraction (HFpEF) shows the strongest association with DM, reflecting shared pathophysiological pathways beyond traditional ischemic heart disease. Epidemiologically, DM confers a two- to four-fold increased risk of incident HF, with a disproportionate burden of HFpEF. Patients with HFpEF exhibit a high prevalence of DM and insulin resistance, accompanied by worse exercise intolerance, higher hospitalization rates, and increased mortality. These observations support the concept that DM is not merely a comorbidity but a central contributor to HFpEF pathogenesis. Mechanistically, chronic hyperglycemia and insulin resistance initiate a cascade of systemic and myocardial abnormalities. Endothelial dysfunction, coronary microvascular inflammation, and impaired nitric oxide–cyclic GMP–protein kinase G signaling promote cardiomyocyte stiffness and diastolic dysfunction. Metabolic inflexibility, characterized by excessive fatty acid utilization and impaired glucose oxidation, reduces myocardial energetic efficiency. In parallel, advanced glycation end products, oxidative stress, mitochondrial dysfunction, and lipotoxicity drive myocardial fibrosis and adverse extracellular matrix remodeling. These myocardial changes are further amplified by extracardiac factors common in DM—obesity, chronic kidney disease, systemic inflammation, and autonomic imbalance—creating the multi-organ HFpEF syndrome. Conversely, HF exacerbates insulin resistance through neurohormonal activation, inflammation, and skeletal muscle hypoperfusion, reinforcing a vicious cycle between metabolic and cardiac dysfunction. Recognition of this cross-talk has important therapeutic implications, as exemplified by sodium–glucose cotransporter 2 inhibitors, which improve HF outcomes through mechanisms extending beyond glucose lowering. In summary, DM and HFpEF are linked through shared mechanistic pathways involving metabolism, microvascular dysfunction, and inflammation. A mechanistic understanding of this interaction is essential for developing integrated, phenotype-specific cardio-metabolic strategies.
Metabolic Dysfunction and Brain Health: Diabetes as a Risk Factor for Dementia

Jong-Ling FuhTaiwan Speaker Metabolic Dysfunction and Brain Health: Diabetes as a Risk Factor for DementiaType 2 Diabetes Mellitus (T2DM) is no longer confined to glucose dysregulation—it is a systemic accelerator of brain aging and a major modifiable risk factor for dementia. Epidemiologic and mechanistic studies reveal that poor glycemic control, including both hyper- and hypoglycemia, significantly increases dementia risk. Data from Taiwan’s National Health Insurance Database show that pronounced glycemic fluctuations more than double this risk, while meta-analyses identify prolonged diabetes duration, elevated HbA1c, hypertension, and insulin resistance as key predictors of cognitive decline. Pathophysiological evidence links chronic hyperglycemia and insulin resistance to neuroinflammation, oxidative stress, and tau pathology. Neuroimaging studies show hippocampal atrophy and white matter degradation in patients with poorly controlled diabetes. Cardiovascular comorbidities amplify this burden: diabetes combined with coronary artery disease doubles the risk of vascular dementia. Encouragingly, therapeutic innovation offers hope. Glucose-lowering agents such as GLP-1 Receptor Agonists (GLP-1RAs) and SGLT2 Inhibitors (SGLT2is) may extend their cardiometabolic benefits to the brain. GLP-1RAs have shown a 45% reduction in dementia risk in real-world and trial-based analyses, reinforcing the interconnectedness of metabolic, vascular, and neurodegenerative pathways. In East Asia, where diabetes and dementia are surging, the clinical imperative is clear: brain health must be a core outcome of metabolic care. Early glycemic optimization, vascular protection, and neuroprotective therapies may define the next frontier in dementia prevention.
Sleep Apnea in Diabetes: A Silent Aggravator

Li-Pang ChuangTaiwan Speaker Sleep Apnea in Diabetes: A Silent AggravatorObstructive sleep apnea (OSA) is a highly prevalent clinical disease affecting more than 10% of the adult population. It is characterized by repetitive episodes of partial or total upper airway obstruction during sleep, resulting in subsequent sleep fragmentation and intermittent hypoxia. Accumulating studies reveal that OSA is an independent risk factor for consequent cardiovascular morbidities, such as myocardial infarction, heart failure, nocturnal dysrhythmias and pulmonary hypertension. Currently, OSA can be treated by means of positive airway pressure therapy, pharmacological therapy and surgical intervention. OSA is a silent aggravator of diabetes because it worsens glucose metabolism and insulin resistance through mechanisms like intermittent hypoxia, sleep fragmentation, and sympathetic nervous system activation. This creates a bidirectional relationship where OSA increases the risk and severity of diabetes, and diabetes can worsen OSA. Treating OSA may improve glycemic control, and screening for it is crucial, especially in individuals with type 2 diabetes, particularly those who are obese.

3F Banquet Hall

Prof.Jong-LingFuh Taiwan

22 MARCH