Amyloid Protein in Dementia

All cells are like minute factories, producing thousands of proteins with precise functions to keep the cells viable. A flaw can occur if a protein is altered, or if excess or too little is formed. Sometimes, the consequences are so severe that a cell dies. Neuron ruination is the chief cause of dementia and is often associated to malfunctions in the connection system that a neuron needs to survive.

Dementia is associated with accumulation of two proteins – amyloid and tau - into plaques and tangles in the brain. Beta-amyloid accumulates as plaques in Alzheimer's disease or dementia and is an endorsement of the disease. Tau compiles into tangles (known as neurofibrillary tangles or NFT). And further disrupts the structure and communication within the nerve cells, leading to cell death.

  • Amyloid Protein and Dementia
  • Accumulation of toxic amyloid β (Aβ)
  • Neurofibrillary tangles
  • Tau Tangles & Beta Plaques
  • Cerebral amyloid angiopathy
  • Amyloid-beta metabolism
  • Potential Treatments towards Aβ Depositions
  • Disruption of Nerve Cells

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