Novel approaches in the understanding of the neurodegeneration observed in Alzheimers disease (AD), involving neurochemical as well as biochemical techniques are being developed, opening up new possibilities in the direction of a metabolic degeneration. Indeed, brain lipids are closely involved in amyloid β-related pathogenic pathways. An important modulator of lipid homeostasis is the pluripotent peptide leptin, which has been shown to reduce amyloid β levels and tau-related pathological pathways, the major pathological hallmarks of AD. These data suggest that leptin holds promise as a novel therapeutic tool for AD. In this article, with some patent literature we will review here some of the most promising approaches involving leptin to cure and prevent, rather than to treat, AD symptoms.
Keywords: Alzheimer's disease, leptin, amyloidosis, hyperphosphorylated tau, neurons, transgenic mice, megalin, choroid plexus, blood-brain barrier, synapses, neuroprotection, neurogenesis, cardiovascular risk factors, obesity, metabolic syndrome
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