Previously, researchers have shown that treating cells with neuregulin - 1, for example, dampens
levels of amyloid precursor protein, a molecule that generates amyloid beta, which aggregate and form plaques in the brains of Alzheimer's patients.
That's because the boosted mice produced normal — rather than high —
levels of the amyloid precursor proteins from which plaques are made.
Not exact matches
There were no differences in CSF
levels of total tau, Aβ42, Aβ40, soluble
amyloid β
protein precursor (sAβPP) α or β, or F2 - isoprostanes.
Aged mutant
amyloid precursor protein mice with established disease showed a near complete restoration in
levels of synaptic and neuronal
proteins after exposure to young blood in parabiosis (synaptophysin P =.02; calbindin P =.02) or following intravenous plasma administration (synaptophysin P <.001; calbindin P =.14).
One hypothesis is that as a regulator
of Amyloid Precursor Protein (APP), a gene that may be partly responsible for inducing Alzheimer's, TSH
levels may have a direct impact on the prevalence
of Alzheimer's.