Image Caption : Alzheimer's Culprit is Beta-Amyloid Plaque
1. Beta amyloid is a protein that is made by cells during normal metabolism. But in AD, there is an abnormal cleavage of this protein in the cell membrane.
2.Beta amyloid can bind to dendrites on nerves and interfere with their normal function.
3.Smaller beta amyloid proteins accumulate to form large plaques between nerve cells.
Also called: AD
Alzheimer's disease (AD) is the most common form of dementia among older people. Dementia is a brain disorder that seriously affects a person's ability to carry out daily activities.
AD begins slowly. It first involves the parts of the brain that control thought, memory and language. People with AD may have trouble remembering things that happened recently or names of people they know. A related problem, mild cognitive impairment (MCI), causes more memory problems than normal for people of the same age. Many, but not all, people with MCI will develop AD.
In AD, over time, symptoms get worse. People may not recognize family members or have trouble speaking, reading or writing. They may forget how to brush their teeth or comb their hair. Later on, they may become anxious or aggressive, or wander away from home. Eventually, they need total care. This can cause great stress for family members who must care for them.
AD usually begins after age 60. The risk goes up as you get older. Your risk is also higher if a family member has had the disease.
No treatment can stop the disease. However, some drugs may help keep symptoms from getting worse for a limited time.
NIH: National Institute on Aging
Amyloid beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are crucially involved in Alzheimer's disease as the main component of the amyloid plaques found in the brains of Alzheimer patients. The peptides result from the amyloid precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ. Aβ molecules can aggregate to form flexible soluble oligomers which may exist in several forms. It is now believed that certain misfolded oligomers (known as "seeds") can induce other Aβ molecules to also take the misfolded oligomeric form, leading to a chain reaction akin to a prion infection. The seeds or the resulting amyloid plaques are toxic to nerve cells. The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold.
A recent study suggested that APP and its amyloid potential is of ancient origins, dating as far back as early deuterostomes.
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