"How and when environmental agents and dietary factors affect the course of Alzheimer's disease: the ""LEARn"" model (latent early-life associated regulation) may explain the triggering of AD."
APP is a large membrane-bound copper-binding protein that is essential in maintaining synaptic function and may play a role in synaptogenesis. beta-Amyloid has been shown to contribute to the oxidative stress that accompanies AD.
Leptin, an adipocytokine involved in cell survival and in learning, has been demonstrated to regulate Abeta production and tau hyperphosphorylation in transgenic mice for AD.
Abeta peptides as one of the crucial volume transmission signals in the trophic units and their interactions with homocysteine. Physiological implications and relevance for Alzheimer's disease.
Abnormally high levels of monoamine oxidase (MAO) activity, which are potentially linked to cytotoxic free radical formation, are known to occur during aging and in neurodegenerative disorders (MAO-B is markedly increased in plaque-associated astrocytes in Alzheimer's disease).
Accumulation of amyloid-beta (Abeta) peptide and deposition of hyperphosphorylated tau protein are two major pathological hallmarks of Alzheimer's disease (AD).
Aging studies in the senescence-accelerated mouse strain (SAM) prone/8 (SAMP8), an animal model of Alzheimer's disease (AD), revealed significantly decreased mRNA and protein expression of AMF and AMFR in the hippocampus.