Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/ijms22115991
Keywords
A beta oligomers; hyperexcitability; excitatory/inhibitory unbalance; synaptic plasticity; network dysfunction; neurotoxicity; calcium homeostasis
Funding
- JPND bPRIDE (blood Proteins for early Discrimination of dEmentias) project
- call JPco-fuND-2: Multinational research projects on Personalised Medicine for Neurodegenerative Diseases (CUP) [J99C18000210005]
- BE-FOR-ERC program (Sapienza University)
- Italian Ministry of Health Ricerca corrente
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Oligomeric A beta proteins exert toxicity through interaction with membrane receptors and formation of ion-permeable channels, affecting synaptic function and network structure.
Amyloid-beta (A beta) 1-40 and 1-42 peptides are key mediators of synaptic and cognitive dysfunction in Alzheimer's disease (AD). Whereas in AD, AP is found to act as a pro-epileptogenic factor even before plaque formation, amyloid pathology has been detected among patients with epilepsy with increased risk of developing AD. Among A beta aggregated species, soluble oligomers are suggested to be responsible for most of A beta's toxic effects. A beta oligomers exert extracellular and intracellular toxicity through different mechanisms, including interaction with membrane receptors and the formation of ion-permeable channels in cellular membranes. These damages, linked to an unbalance between excitatory and inhibitory neurotransmission, often result in neuronal hyperexcitability and neural circuit dysfunction, which in turn increase A beta deposition and facilitate neurodegeneration, resulting in an A beta-driven vicious loop. In this review, we summarize the most representative literature on the effects that oligomeric A beta induces on synaptic dysfunction and network disorganization.
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