Not exact matches
The bulk
of research scientists working on Alzheimer's have long believed that a
buildup of amyloid «plaques» is central to the disease's development — and that therefore targeting this
protein is the best chance for a cure.
For one, it would give them three specific biological markers to hone in on: The
buildup of beta
amyloid and tau
proteins, which cause brain plaques associated with Alzheimer's, and brain nerve cell death.
According to the proposal, called the
amyloid hypothesis, Alzheimer's disease, estimated to affect more than 5 million people in the United States alone, is caused by abnormal
buildup of A-beta
protein in the brain.
Recent research also has illuminated how the deadly cascade that leads to brain atrophy is set in motion: The
buildup of amyloid plaques, working in tandem with certain gene mutations, sparks the formation
of the renegade tau
proteins.
Researchers have proposed that Alzheimer's disease is caused by the
buildup of a sticky
protein called beta -
amyloid.
Like cardiovascular disease, Alzheimer's involves the
buildup of plaque, in this case tangled beta -
amyloid proteins in the brain.
It not only prevented the
buildup of amyloid beta (Aß), a sticky
protein linked to Alzheimer's, but it also does not appear to produce the dangerous side effects
of earlier versions tested in humans.
«Activation
of these cell receptors appear to prevent brain cells from cleaning out the trash — the toxic
buildup of proteins, such as alpha - synuclein, tau and
amyloid, common in neurodegenerative diseases,» says the study's senior author, neurologist Charbel Moussa, MBBS, PhD, director
of Georgetown's Laboratory for Dementia and Parkinsonism, and scientific and clinical research director
of the GUMC Translational Neurotherapeutics Program.
More than 40 illnesses known as
amyloid diseases — Alzheimer's, Parkinson's and rheumatoid arthritis are a few — are linked to the
buildup of proteins after they have transformed from their normally folded, biologically active forms to abnormally folded, grouped deposits called fibrils or plaques.
Spinal fluid analyses and positron emission tomography (PET) scans can detect a key warning sign —
buildup of amyloid - beta
protein in the brain.
Many neuroscientists believe that a
buildup in the brain
of a
protein fragment called beta -
amyloid causes Alzheimer's disease.
The disease is largely attributed to an abnormal
buildup of proteins, which can form
amyloid beta plaques and tangles in the brain that trigger inflammation and result in the loss
of brain connections called synapses, the effect most strongly associated with cognitive decline.
The new therapy targets beta - secretase, an enzyme on neurons around which plaques (
buildups of a
protein called beta -
amyloid) cluster in the brain.
The DNA change may inhibit the
buildup of β
amyloid, the
protein fragment that accumulates in the hallmark plaques that form in the brains
of Alzheimer's patients.
While the
buildup of sticky
proteins called
amyloid plaques in the brain has been repeatedly linked to Alzheimer's disease, the role
of blood in the formation
of the condition has been less clear.