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19th International Conference on Dementia and Alzheimer Disease, will be organized around the theme “Neurological Advancements: Revolutionizing Alzheimer's Diagnosis and Treatment”

Euro Dementia 2025 is comprised of keynote and speakers sessions on latest cutting edge research designed to offer comprehensive global discussions that address current issues in Euro Dementia 2025

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Alzheimer’s disease is a progressive neurodegenerative disorder that primarily affects memory, thinking, and behavior. It is the most common cause of dementia. It is characterized by the accumulation of amyloid plaques and tau tangles in the brain, leading to the death of brain cells. Risk factors include age, genetics, and lifestyle factors. While there is no cure, treatments aim to manage symptoms and slow progression. Alzheimer's is a growing global health challenge, with an estimated 44 million people affected worldwide, a number expected to double by 2050. Early diagnosis and ongoing research are crucial for improving patient outcomes.

Vascular Dementia is the second most common type of dementia, caused by reduced blood flow to the brain due to damage to blood vessels. This disruption in circulation leads to brain cell death, affecting cognitive function, memory, and decision-making. Vascular dementia often results from strokes, either major or mini (transient ischemic attacks), or from other conditions that damage the blood vessels, such as high blood pressure, diabetes, and high cholesterol.

Symptoms of vascular dementia can vary but commonly include memory loss, confusion, difficulty concentrating, and problems with planning or organizing tasks. Unlike Alzheimer's, vascular dementia symptoms may appear suddenly, often following a stroke or series of strokes.

Parkinson’s disease (PD) is a neurodegenerative disorder that primarily affects movement, causing tremors, stiffness, and difficulty with balance and coordination. Over time, some individuals with Parkinson's may develop Parkinson’s disease dementia (PDD), a form of dementia that affects cognitive function, including memory, attention, and executive function. The progression of Parkinson's disease can lead to changes in the brain's dopamine systems, which can also impact areas responsible for cognition. Symptoms of PDD include memory loss, difficulty with problem-solving, and personality changes.

The pathophysiology of dementia involves the progressive degeneration of brain cells, leading to impaired cognitive function. In Alzheimer's disease, the most common cause of dementia, amyloid plaques (abnormal protein clumps) and tau tangles (twisted protein fibers) disrupt communication between neurons, causing cell death. In vascular dementia, reduced blood flow due to damaged blood vessels results in brain cell death, often following strokes. Other types, like Parkinson’s disease dementia, involve the loss of dopamine-producing neurons, affecting both movement and cognition.

The underlying pathophysiological changes in dementia often lead to a decline in memory, judgment, reasoning, and the ability to perform daily tasks. These neurodegenerative processes are still not fully understood, and ongoing research aims to identify mechanisms for early diagnosis and treatment.

Dementia and Nutrition are closely linked, as a healthy diet can support brain function and potentially reduce the risk of cognitive decline. Diets rich in antioxidants, omega-3 fatty acids, and anti-inflammatory nutrients have been shown to benefit brain health. For example, the Mediterranean diet, which includes fruits, vegetables, whole grains, healthy fats, and fish, has been associated with a lower risk of dementia. Similarly, diets high in vitamins such as B12, D, and folate are crucial for cognitive function. Conversely, diets high in processed foods, sugars, and unhealthy fats may contribute to neuroinflammation and vascular damage, which can accelerate cognitive decline. Proper nutrition, along with regular physical activity, is essential for maintaining brain health and potentially delaying the onset of dementia.

Alzheimer's disease therapeutics focus on managing symptoms and slowing disease progression, though there is no cure. Current treatments include acetylcholinesterase inhibitors (e.g., donepezil) to improve neurotransmission and temporarily alleviate cognitive symptoms. NMDA antagonists (e.g., memantine) help regulate glutamate activity, which is involved in learning and memory. Recent advancements include monoclonal antibodies targeting amyloid plaques (e.g., aducanumab), aimed at reducing the buildup of toxic proteins in the brain. Research is also exploring gene therapy, anti-inflammatory treatments, and lifestyle interventions to prevent or delay the onset. Early diagnosis and personalized care are key to optimizing therapeutic outcomes.

Neuro-inflammation plays a critical role in the development and progression of dementia, including Alzheimer’s disease. Inflammation in the brain is often triggered by the accumulation of amyloid plaques and tau tangles, which activate the immune system’s microglia and astrocytes. While these cells initially protect the brain, chronic activation leads to neuroinflammation, causing neuronal damage and impairing cognitive function.

The immune response in dementia also involves the disruption of the blood-brain barrier and increased release of pro-inflammatory cytokines. Targeting neuroinflammation is a promising area of research, with potential therapies aimed at modulating the immune system to slow disease progression and improve brain health.

Geriatrics and dementia care focus on supporting older adults with cognitive decline, addressing both medical and emotional needs. Care involves managing chronic conditions, optimizing medications, and ensuring patient safety. It also includes cognitive stimulation, behavioral management, and providing caregiver support. The aim is to improve quality of life through a holistic approach, considering both physical and mental health, while assisting families in navigating the challenges of caregiving for individuals with dementia.

Alzheimer's disease and co-morbidities often occur together, complicating diagnosis and treatment. Common co-existing conditions include cardiovascular diseases, diabetes, depression, and stroke, which can worsen cognitive decline. For instance, hypertension and diabetes contribute to vascular damage, increasing Alzheimer's risk. Depression and sleep disorders are also prevalent, affecting mood and cognitive function. Other conditions like Parkinson’s disease and nutritional deficiencies can further impair memory and daily functioning.

Memory disorders and cognitive dysfunction refer to impairments in memory, thinking, and problem-solving abilities. These conditions can result from various causes, including Alzheimer's disease, vascular dementia, Parkinson's disease, and traumatic brain injury. Memory issues can range from mild forgetfulness to severe cognitive decline, affecting daily functioning. Cognitive dysfunction may include difficulties with attention, decision-making, and language. Early detection and intervention are essential for managing these disorders, often involving a combination of medications, cognitive therapies, and lifestyle changes to improve cognitive function and quality of life.

Dementia and diabetes are closely linked, with diabetes increasing the risk of cognitive decline and dementia. High blood sugar levels can damage blood vessels, leading to vascular dementia, while insulin resistance may contribute to Alzheimer’s disease by impairing brain function. Managing diabetes through diet, exercise, and medication is crucial to reduce the risk of cognitive deterioration.

Neuroimaging in dementia plays a crucial role in diagnosing and monitoring neurodegenerative diseases. Techniques such as MRI (Magnetic Resonance Imaging) and CT (Computed Tomography) scans help identify structural brain changes, including atrophy and lesions. Advanced imaging methods like PET (Positron Emission Tomography) and SPECT (Single Photon Emission Computed Tomography) can detect abnormal protein deposits, such as amyloid plaques in Alzheimer's disease. Neuroimaging aids in early diagnosis, differentiating between types of dementia, and tracking disease progression for better treatment planning.

Childhood trauma has been linked to an increased risk of developing dementia in later life. Adverse experiences such as abuse, neglect, or prolonged stress can affect brain development, leading to long-term changes in brain structure and function. Chronic stress from trauma may contribute to neuroinflammation and cognitive decline, raising the likelihood of neurodegenerative diseases like Alzheimer's. These early life experiences can significantly impact brain health and dementia risk in adulthood.

Early diagnosis of dementia is crucial for effective intervention and slowing disease progression. Advances in biomarkers—biological indicators of disease—are enhancing diagnostic accuracy and enabling earlier detection. Biomarkers for dementia include amyloid plaques and tau protein tangles in Alzheimer's disease, detectable through PET scans or cerebrospinal fluid analysis. Additionally, genetic markers, neuroimaging (MRI, fMRI), and blood-based tests are being researched for their potential to identify dementia at its earliest stages. Early detection allows for timely treatment, better management of symptoms, and improved outcomes for patients and caregivers.

Clinical features of dementia include memory loss, confusion, and difficulty with communication, impaired judgment, and changes in mood or behavior. As dementia progresses, individuals may struggle with daily tasks, mobility, and coordination. Physiotherapy plays a key role in managing these symptoms by improving physical function, enhancing mobility, and reducing the risk of falls. Tailored exercise programs can help maintain strength, balance, and flexibility, while promoting overall well-being and improving the quality of life for dementia patients.

Medical biotechnology is playing an increasingly vital role in the understanding and treatment of Alzheimer’s disease. Innovations in biotechnology have led to the development of biomarkers for early diagnosis, including blood tests and imaging techniques that detect amyloid plaques and tau tangles. Advances in gene therapy and stem cell research hold promise for potentially reversing or halting disease progression. Additionally, biotechnological breakthroughs in targeted drug development, such as monoclonal antibodies (e.g., aducanumab), aim to reduce amyloid buildup in the brain. These innovations offer hope for more effective treatments and better outcomes for Alzheimer's patients.

Amyloid protein accumulation is a hallmark of Alzheimer's disease and other forms of dementia. The buildup of amyloid plaques between neurons disrupts cell communication, leading to neurodegeneration and cognitive decline. Amyloid-related changes are central to the disease’s pathophysiology, making it a key target for diagnostic biomarkers and therapeutic strategies aimed at slowing or halting disease progression.

Ageing is the primary risk factor for dementia, with the likelihood of developing neurodegenerative diseases like Alzheimer's increasing with age. As the brain ages, it undergoes changes in structure and function, including the buildup of amyloid plaques and tau tangles. These changes can impair cognitive function, leading to memory loss, confusion, and other symptoms of dementia. The growing aging population worldwide makes dementia a major public health challenge, emphasizing the need for early detection, prevention strategies, and effective care solutions.

Genomic medicine in Alzheimer's disease explores the role of genetic factors in the development and progression of the disease. Research has identified several genes linked to Alzheimer's, such as APOE4, which increases the risk, and APP, PSEN1, and PSEN2 genes, which are associated with early-onset forms of the disease. Advances in genomic technologies, including whole-genome sequencing and gene editing, are paving the way for personalized treatments and early diagnosis. By understanding genetic risk factors, genomic medicine holds promise for identifying individuals at risk, developing targeted therapies, and potentially preventing or slowing Alzheimer's disease progression.

The neuropathology of Alzheimer's disease is characterized by the accumulation of amyloid plaques and neurofibrillary tau tangles in the brain. These abnormal protein deposits disrupt neuronal communication, trigger inflammation, and cause neuronal death. Over time, this leads to brain atrophy, memory loss, and cognitive decline, which are hallmark features of the disease.

Pharmacological advances in dementia treatment focus on developing drugs to slow disease progression and manage symptoms. Current medications for Alzheimer’s disease, such as acetylcholinesterase inhibitors (e.g., donepezil) and NMDA antagonists (e.g., memantine), help improve cognitive function temporarily. Recent breakthroughs include monoclonal antibodies, like aducanumab, which target amyloid plaques to reduce protein buildup in the brain. Other promising areas of research involve tau-targeted therapies, anti-inflammatory drugs, and gene therapies. These innovations aim to address the underlying causes of dementia, offering hope for more effective treatments and, eventually, potential disease-modifying options.