Cytoskeleton-related Alzheimer’s Disease Research Service

Mechanisms of Alzheimer’s Disease

Alzheimer’s disease continues to destroy brain tissue, causing patients to lose memory and experience disorientation, among other things, potentially rendering them unable to care for themselves in their daily lives. With in-depth knowledge of cytoskeleton-related research services and extensive project experience, we provide reference materials on Alzheimer’s Disease to help you learn more about our various testing services and welcome you to contact us directly for more specific solutions.

Alzheimer’s disease (AD) is the leading cause of dementia and is a progressive neurodegenerative disease. Dementia includes memory loss and difficulties with thinking, language, and problem-solving skills.

  • Aβ Plaque Associated Neurodegeneration: Aβ plaques form and are deposited in different areas of the brain. These plaques are recognized by the brain as foreign bodies and trigger inflammatory and immune responses by activating microglia and releasing cytokines, ultimately leading to cell death and neurodegeneration.
  • Neurofibrillary Degeneration: Over-activation of cyclin-dependent kinase 5 (CDK5) and leads to tau hyperphosphorylation. Hyperphosphorylation leads to a decrease in the affinity of tau proteins for microtubules. The hyperphosphorylated tau forms NFTs and is deposited in the cytoplasm where it no longer functions to maintain cellular structure.
  • Neuroinflammation: Neuro-inflammation plays a central role in the pathogenesis of AD. Acute inflammation has a protective role in defending against brain injury such as the presence of Aβ plaque.

The Abnormal tau Modification Theory of Alzheimer’s Disease

TAU protein is a microtubule-associated protein. Under normal conditions phosphorylated tau protein binds to microtubules, helps maintain their dynamic stability, and plays an important role in neuronal material transport and information transmission.

The abnormal modification of tau protein in Alzheimer’s disease is believed to be the result of hyperphosphorylation, which weakens the ability of tau protein to bind to microtubule proteins, destroying the cytoskeleton and producing abnormal neurofibrillary tangles (NFTs) that can be observed under light microscopy, while the microtubules are unable to transport relevant substances due to deformation, and the axons and dendrites of distal neurons atrophy due to lack of nutrients, thus triggering Alzheimer’s disease. Alzheimer’s disease.

Tau and Aβ PET images in cognitively healthy controls (top-CDR0) and AD patientsTau and Aβ PET images in cognitively healthy controls (top-CDR0) and AD patients (bottom-CDR>0) [1].

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