(6,7) These diagnostic guidelines provide 4 levels of "AD neuropathologic change," based on the ordinal scale ranking of 3 characteristic AD-associated neuropathologies: neuritic plaque
densities, neurofibrillary tangle (NFT) anatomic distribution, and the distribution of parenchymal deposits of [beta]-amyloid peptides (A[beta]).
Neuraceq[TM] can be used to estimate the density of ?-amyloid neuritic plaque
deposition in the brain.
For instance, Sojkova et al reported that in 6 participants, though there was agreement between in-vivo imaging and a neuritic plaque
score for those patients with high or negligible A[beta] levels in vivo, only limited agreement was observed for those with intermediate levels of A[beta], emphasizing the need for better understanding of the correlation between imaging and pathologic assessment.
"Yet the same agency is challenging the value of the only technology approved by the Food and Drug Administration for estimating beta-amyloid neuritic plaque
density in the living brain."
Amyvid works by measuring the beta-amyloid neuritic plaque
density within the brain.
This marketing authorisation is for Amyvid as a diagnostic radiopharmaceutical indicated for Positron Emission Tomography (PET) imaging of beta-amyloid neuritic plaque
density in the brains of adult patients with cognitive impairment who are being evaluated for Alzheimer's disease and other causes of cognitive impairment.
Following diagnosis, neuropathological classification is assessed against A[beta], NFT, and neuritic plaque
methodologies [81-83] to obtain a combined score, those Hyman et al.
They studied mice that carried a genetic mutation for promoting increased amounts of amyloid beta, a protein fragment found within the telltale neuritic plaque
, or "hardening of the brain," seen in Alzheimer's disease.
One notion is that accumulation of amyloid, a protein substance in neuritic plaque
, may cause damage to neurons. In addition, damage to neurons causes a reduction in acetylcholine (ACh), a neurotransmitter that is necessary for relaying messages among the billions of nerve cells in the brain.
Another hypothesis, according to Stanley Rapoport of the National Institute of Aging in Bethesda, Md., is that neuritic plaque
formation may be a result of overcompensation to replace degenerating nerves through accelerated nerve growth.