About this Research Topic
Because of the less significant correlations between the extent of amyloid β deposition and either degree of synapse pathology, neuronal loss or dementia, we are now obliged to conclude that the ‘amyloid β hypothesis’ has become less reliable. Most researchers still place Aβ as central to Alzheimer's disease, although the many possible Aβ-independent disease pathways could also be involved. Since the brain is rich in polyunsaturated fatty acids and harbors a relatively high concentration of oxygen in the lipid bilayer, oxidative stress-induced lipid peroxidation and accumulation of aldehyde products may also be a key factor in neurodegeneration. In this Research Topic, we raise critical questions regarding the role of Aβ in the diagnosis, pathogenesis, and therapeutic strategies for Alzheimer’s disease, as well as consider how oxidative stress, brain ischemia, and alcohol may be implicated.
To this aim, we welcome both Original Research and Review articles focused on the following aspects:
1) New data surrounding the accuracy of current consensus diagnostic criteria for Alzheimer’s disease and the validity of the amyloid hypothesis supporting them.
2) Research into treatment, prediction, diagnosis and etiology in clinically identified Alzheimer subjects irrespective of risk factors.
3) Future investment in longitudinal biomarkers such as neuroinflammation, vascular factors, lipid peroxidation, and synaptic/neurodegeneration markers.
4) Studies of the mechanistic drivers underlying synapse dysfunction and loss.
Keywords: amyloid hypothesis, Alzheimer's disease, dementia, lipid peroxidation, aldehyde, oxidative stress, alcohol, brain ischemia
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