IMR Press / JIN / Special Issues / 1636017615577

Understanding the mechanisms and interactions of amyloid beta aggregates, APOE4, and fatty acids in AD pathogenesis and intervention

Submission deadline: 31 May 2022
Special Issue Editors
Qiu-Lan Ma, MD, PhD
Department of Neurology, David Geffen School of Medicine, University of California in Los Angeles, Los Angeles, CA, USA; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, USA
Interests: Alzheimer’s disease; neurodegenerative diseases; tauopathies; protein misfolding; neuroimmunomodulation; neuroinflammation; neuroprotection; preclinical intervention for drug discovery with cellular and animal models in Alzheimer’s disease and other neurodegenerative diseases
Special Issue and Collections in IMR journals
Special Issue Information

Dear Colleagues, 

Alzheimer’s disease (AD) is the most common neurodegenerative disease of aging. It is characterized pathologically by progressive amyloid deposition, neurofibrillary tangles, and loss of synapses and neurons in specific brain regions. The disease is manifested clinically by progressive loss of learning and memory. It is widely believed that elevated brain amyloid beta (Aβ) directly contributes to the pathogenesis of AD, in which misfolded Aβ aggregates play crucial roles. For decades, although Aβ has been extensively studied in AD pathogenesis, the precise mechanisms of Aβ-induced neurodegeneration remain not entirely understood. This research topic aims to deeply understand the mechanisms of Aβ in AD pathogenesis, which could contribute to the discoveries of novel therapeutic targets in AD. 
Currently, there are no effective drugs to prevent or treat AD. Sporadic AD (SAD) accounts for 90-95% of cases. Both genetic and environmental factors play important roles in the etiology and pathology of SAD. This research topic aims to understand the impact of non-modifiable genetic factors and modifiable environmental factors on AD intervention. For instance, APOE4 is the strongest genetic risk factor for AD. It regulates cholesterol metabolism and accelerates Aβ pathology. The environmental factor of dietary fatty acids can affect a wide variety of physiological and pathological processes in human body. For decades, available evidence from epidemiological, pre-clinical, and clinical studies suggests the preventive and therapeutic effects of omega-3 fatty acid DHA on AD. However, the outcomes are inconsistent. In addition, the beneficial effect of DHA in AD is affected by APOE isoforms with favoring APOE4 non-carriers. Thus, it is important to better understand the mechanisms of the interactions between AD risk genes and dietary intake of fatty acids in AD intervention. Modifiable intake of fatty acids approach could be a promising strategy to prevent or slow the progression of AD.
This research topic welcomes articles that contribute to better understanding the mechanisms and interactions of Aβ, APOE4, and fatty acids in AD pathogenesis and intervention.  
Dr. Qiu-Lan Ma

Guest Editor

Keywords
Alzheimer’s disease
Amyloid beta
Protein misfolding
APOE4
Fatty acids
Manuscript Submission Information

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