Alzheimers Disease & Dementia

Molecular Neurodegeneration & Protein Misfolding Dynamics

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.