In this video, we have explained the #pathophysiology and causes of #Alzheimer's #disease.
A German scientist named Alice Alzheimer discovered irregularities in the brain parts of a dementia patient over a century ago. Since then, scientists have been investigating the unusual plaques and tangles he observed in the hopes of one day understanding and curing Alzheimer's disease.

A peptide termed amyloid beta or a beta forms plaques or intractable deposits. When two enzymes, beat up and gamma secretaries, work together to remove a molecule called amyloid precursor protein, This cleavage produces other compounds that may play a function in the disease. However, A-beta is the main offender. A beta has a proclivity for misfolding and becoming sticky. They eventually form soluble oligomers when they clump together.

These mechanisms eventually damage the neurons. Another issue that has been shown in animal models is that misfolded town proteins can travel across synapses into healthy neurons, causing healthy tower proteins to misfold and disseminate pathology throughout the brain. The pattern of spreading through distinct brain regions corresponds to the shifting symptoms of Alzheimer's disease as it progresses from early to late stages.

This pattern also illustrates how some neurons are more susceptible to death than others. Despite these advancements in our knowledge of Alzheimer's disease, there is no cure. While medications to target amyloid beta or Tao are being researched, it is unknown whether they will ever be effective in treating the condition. Only one thing is certain: basic and clinical research will continue to be supported.

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