Call for Abstract

20th International Conference on Alzheimers Disease & Dementia, will be organized around the theme “Neurorestorative Dementia Science: Precision Biomarkers, Brain-Repair Pathways & AI-Enabled Cognitive Care”

Dementia-2026 is comprised of keynote and speakers sessions on latest cutting edge research designed to offer comprehensive global discussions that address current issues in Dementia-2026

Submit your abstract to any of the mentioned tracks.

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Exploration of neurorestorative pathways focuses on how the brain repairs synaptic structures damaged during Alzheimer’s progression. Research highlights mechanisms such as neurotrophic signaling, synaptic plasticity modulation, and mitochondrial stabilization to restore neuronal communication. Scientists are now decoding molecular repair signatures that guide axonal regrowth, dendritic spine regeneration, and enhanced neurotransmission efficiency. Emerging therapeutics include synaptic modulators, growth-factor mimetics, and neurorestoration-inducing peptides capable of reversing early structural damage. Preclinical models demonstrate improved memory circuits by enhancing long-term potentiation and rebuilding disrupted neural networks. Combining bioengineering, stem-cell–derived exosomes, and pharmacologic boosters is offering new avenues to promote robust synaptic recovery. Understanding how neurodegeneration disrupts these mechanisms enables the creation of targeted interventions that strengthen resilience in vulnerable regions such as the hippocampus and cortex. Neurorestorative science provides a foundation for disease-modifying treatments aimed not only at slowing decline but also improving functional cognition, independence, and long-term brain health in individuals affected by Alzheimer’s disease.

Precision biomarker research is transforming the ability to detect Alzheimer’s disease years before symptoms arise. Advanced blood-based markers, CSF signatures, polygenic risk scores, and digital biomarkers offer highly sensitive indicators of early pathology. Predictive neuroanalytics leverages AI algorithms to track subtle cognitive fluctuations, speech patterns, retinal changes, and gait abnormalities, enabling a more accurate forecast of progression. Novel biomarkers, including phosphorylated tau isoforms, neurofilament light chain, and synaptic proteins, provide comprehensive mapping of neuronal injury and misfolding processes. Imaging biomarkers such as amyloid-PET, tau-PET, and volumetric MRI are increasingly used to quantify disease burden and predict trajectory. The integration of multi-omics approaches genomics, proteomics, metabolomics supports personalized disease-risk profiling. These innovations empower clinicians to intervene earlier, refine therapeutic planning, and stratify patients for clinical trials with greater accuracy. As precision diagnostics evolve, they offer new possibilities for monitoring treatment response, developing targeted therapies, and fundamentally reshaping the landscape of Alzheimer’s prevention and early detection.

Artificial intelligence is reshaping dementia diagnostics by enabling continuous, real-time monitoring of cognitive health. AI-driven tools analyze speech, behavior, writing patterns, navigation habits, and digital device interaction to detect early cognitive impairment long before traditional assessments. Machine learning algorithms can identify micro-patterns in memory lapses, reaction times, decision-making, and emotional signals, providing highly accurate and dynamic cognitive profiling. Digital platforms, smartphone-based screening, and wearable sensors generate objective, high-frequency data streams that support remote diagnosis and longitudinal tracking. AI-powered risk scoring systems integrate medical history, imaging data, and biomarker profiles to create personalized disease trajectories. These innovations improve accessibility to diagnostic care, especially for patients in remote or underserved regions. Digital intelligence enhances clinical decision-making, supports timely intervention, and improves adherence to therapeutic plans. As AI models grow more interpretable and clinically validated, they offer powerful support for clinicians and caregivers, optimizing early detection, treatment adjustment, and patient engagement throughout the continuum of dementia care.

The study of molecular neurodegeneration examines how misfolded proteins such as amyloid-β and tau disrupt neuronal integrity and accelerate Alzheimer’s pathology. Misfolding, aggregation, and propagation across neural circuits trigger synaptic loss, mitochondrial dysfunction, oxidative stress, and inflammatory cascades. Research focuses on identifying the earliest molecular triggers of plaque formation, tau hyperphosphorylation, and neurofibrillary tangle spread. Advanced structural biology, cryo-EM imaging, and molecular modeling are providing unprecedented insights into protein conformational changes and toxic oligomer formation. Therapeutic strategies are increasingly targeting protein clearance mechanisms, including autophagy enhancement, proteasome activation, and chaperone-mediated stabilization. Interrupting aggregation pathways may halt or reverse neuronal injury. Understanding misfolding kinetics and transmission mechanisms supports development of next-generation therapies capable of slowing progression and preserving cognitive function. Molecular insights remain foundational for creating disease-modifying treatments that directly address the root biology of Alzheimer’s disease.

Genomic and epigenomic research is uncovering the underlying factors that shape Alzheimer’s susceptibility, onset, and progression. Key genetic contributors, including APOE variants, TREM2 mutations, and polygenic risk factors, help explain individual differences in disease vulnerability. Epigenomic changes such as DNA methylation, histone modification, and chromatin remodeling alter gene expression patterns linked to inflammation, synaptic health, and metabolic dysfunction. Environmental influences including stress, lifestyle, and toxin exposure can further modify epigenetic signatures, accelerating neurodegenerative processes. Advances in single-cell sequencing and spatial transcriptomics reveal cell-specific regulatory changes occurring in neurons, astrocytes, and microglia during disease evolution. Understanding these mechanisms enables precision profiling and supports development of targeted therapies that modulate gene expression pathways. Gene-editing tools, epigenetic modulators, and personalized risk assessment models hold promise for predicting progression and designing individualized treatment strategies rooted in genetic and regulatory biology.

Neuroinflammation plays a central role in Alzheimer’s disease, with microglia acting as key regulators of immune responses in the brain. Dysfunctional microglial activation contributes to synaptic loss, amyloid accumulation, and accelerated neurodegeneration. Research is advancing understanding of how cytokine signaling, inflammasome activity, and immune-mediated oxidative stress shape disease progression. Modulating microglial phenotypes shifting them from pro-inflammatory to neuroprotective states offers promising therapeutic potential. Novel drugs, monoclonal antibodies, and small molecules are being developed to regulate immune signaling pathways and restore balanced neuroimmune responses. Neuroinflammation biomarkers are increasingly used to stratify patients and guide personalized therapy decisions. Integrating immune modulation with other therapeutic strategies enhances the potential to slow cognitive decline and protect structural brain integrity.

Next-generation therapeutics targeting amyloid and tau are reshaping the landscape of Alzheimer’s treatment. New anti-amyloid antibodies, tau aggregation inhibitors, small-molecule stabilizers, and dual-pathway modulators aim to reduce neurotoxic buildup and preserve neural networks. These therapies combine improved safety profiles with precision dosing and biomarker-guided monitoring. Advances in drug delivery systems increase blood–brain barrier penetration, maximizing therapeutic impact. Combination therapies that simultaneously target amyloid, tau, and inflammatory pathways show promise in modifying disease trajectories. Continuous clinical research is refining efficacy, identifying ideal treatment windows, and enabling earlier intervention. These innovations signal a major shift toward disease-modifying approaches capable of addressing core pathology.

Brain connectomics investigates how Alzheimer’s disrupts communication across neural networks. Advanced imaging reveals alterations in structural and functional connectivity within memory, attention, and executive processing circuits. Researchers map how signal transmission deteriorates as synapses fail, white-matter tracts degrade, and long-range communication becomes inefficient. Computational models simulate network breakdown and identify key nodes most vulnerable to early damage. These insights guide development of targeted therapies that restore connectivity through neurostimulation, behavioral training, and pharmacologic enhancement. Connectomic mapping provides precise biomarkers for progression, enabling personalized monitoring and intervention strategies.

Lifestyle and nutritional interventions play growing roles in delaying Alzheimer’s onset and promoting neuroprotective aging. Diet patterns such as MIND, Mediterranean, and ketogenic diets influence brain metabolism, inflammation, and oxidative balance. Physical activity enhances synaptic plasticity, improves vascular health, and increases neurotrophic factor expression. Sleep optimization, stress management, cognitive training, and social engagement support long-term brain resilience. Integrating lifestyle science with personalized risk profiles empowers individuals to adopt evidence-based prevention strategies.

Vascular dysfunction significantly contributes to cognitive impairment, interacting with amyloid and tau pathology to accelerate decline. Reduced cerebral perfusion, microvascular injury, and endothelial dysfunction damage neurons and impair metabolic efficiency. Research explores therapeutic approaches including vascular-targeted drugs, antihypertensives, antithrombotics, and lifestyle interventions that improve cerebrovascular integrity. Identifying early vascular biomarkers supports intervention long before cognitive symptoms emerge.

Modern neuroimaging tools provide unmatched visibility into Alzheimer’s progression. High-resolution MRI quantifies structural atrophy, while PET imaging maps amyloid, tau, and neuroinflammation. Multimodal approaches integrate metabolic, functional, and molecular imaging for comprehensive brain analysis. AI-enhanced imaging improves diagnostic accuracy, disease staging, and treatment-response assessment.

Digital therapeutics are transforming dementia rehabilitation through interactive training, VR-based exercises, and remote cognitive therapy. Personalized digital protocols stimulate memory circuits, support motor planning, and promote cognitive engagement. Remote care platforms increase accessibility, reduce caregiver burden, and enable consistent long-term monitoring.

Behavioral and psychiatric symptoms significantly affect Alzheimer’s outcomes. Understanding neural mechanisms behind agitation, anxiety, hallucinations, and mood disorders supports development of targeted interventions. Integrative care models combine medication, behavioral therapy, and environmental adjustments to improve quality of life.

Caregiver support is essential for managing long-term dementia care. Effective models emphasize education, emotional support, respite services, and decision-making tools. Dementia-friendly systems integrate community planning, specialized clinical pathways, and coordinated care frameworks to enhance patient and caregiver well-being.

Drug discovery in Alzheimer’s is accelerating through high-throughput screening, AI modeling, and human-relevant cellular systems. Translational neuroscience bridges laboratory findings with clinical testing, improving trial design and patient selection. Innovations aim to reduce failure rates, optimize dosing, and bring disease-modifying therapies to patients faster.