They injected tiny
amounts of amyloid protein into the brains of the monkeys and found that old Rhesus monkeys developed Alzheimer's - like symptoms but young monkeys stayed healthy.
Not exact matches
Because PIB selectively binds to brain
amyloid deposits but quickly clears from normal tissue, the chemical dye accurately indicates the
amount of protein that is deposited in the living brain.
While these compounds did not reduce the
amount of protein aggregates, they were found to reduce the
protein's toxicity and to increase the stability
of amyloid fibrils — a finding that lends further evidence to the theory that smaller assemblies
of amyloid - beta known as oligomers, and not the fibrils themselves, are the toxic agents responsible for Alzheimer's symptoms.
If even trace
amounts of pathogenic
protein are present, they rapidly use the normal
proteins to create millions
of insoluble, fibrous
amyloid strands.
Previous efforts at early detection have focused on beta
amyloid, a
protein found in abnormally high
amounts in the brains
of people with Alzheimer's disease.
The drug also appeared to reduce the
amount of the
protein amyloid beta (which forms toxic plaques in the brains
of Alzheimer's patients) by decreasing the levels
of metals such as zinc and copper.
The
amount of beta -
amyloid proteins, which make up the characteristic Alzheimer's plaques, was also much lower in the brains
of the mice on the low - calorie diet.
Some studies suggest that Alzheimer's patients have an abnormally high
amount of aluminum in the
amyloid protein plaques that characterize the disease, although the exact connection remains unclear.
In this condition, abnormal
amounts of a fibrous
protein substance (
amyloid) collect — for unknown reasons — in otherwise healthy kidney tissue.