Affiliations: [a] Institute of Neuroscience and Physiology, Department of Physiology, the Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden | [b] Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden
Correspondence:
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Corresponding authors: Henrik Zetterberg, MD, PhD, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, S-431 80 Mölndal, Sweden. Tel.: +46 31 343 0142; Fax: +46 31 343 2426; E-mail: [email protected]. Eric Hanse, MD, PhD, Institute of Neuroscience and Physiology, Department of Physiology, the Sahlgrenska Academy at University of Gothenburg, S-405 30 Gothenburg, Sweden. Tel.: +46 31 786 3510; Fax: +46 31 786 3505; E-mail: [email protected].
Abstract: Pathological hallmarks of Alzheimer's disease (AD) include synaptic and neuronal degeneration and the presence of extracellular deposits of amyloid-β (Aβ) in senile plaques in the cerebral cortex. Although these brain lesions may be seen also in aged non-demented individuals, the increase in brain Aβ is believed by many to represent the earliest event in the disease process. Accumulating evidence suggests that Aβ, which is highly conserved by evolution, may have an important physiological role in synapse elimination during brain development. An intriguing idea is that this putative function can become pathogenic if activated in the aging brain. Here, we review the literature on the possible physiological roles of Aβ and its precursor protein AβPP during development with special focus on electrophysiological findings.
