Amyloidogenic protein aggregation is a pathological hallmark of Alzheimer's Disease (AD). As such, this critical feature of the disease has been instrumental in guiding research on the mechanistic basis of disease, diagnostic biomarkers and preventative and therapeutic treatments. Here we review identified molecular triggers and modulators of aggregation for two of the proteins associated with AD: amyloid beta and tau. We aim to provide an overview of how specific molecular factors can impact aggregation kinetics and aggregate structure to promote disease. Looking toward the future, we highlight some research areas of focus that would accelerate efforts to effectively target protein aggregation in AD.
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| http://dx.doi.org/10.1016/j.neurot.2024.e00512 | DOI Listing |
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Article Synopsis
- Parkinson's disease (PD) is characterized by the loss of dopamine neurons and is influenced by α-synuclein aggregation and neuroinflammation, with microglia playing a key role.
- Previous research identified mesencephalic astrocyte-derived neurotrophic factor (MANF) as a potential inhibitor of α-synuclein accumulation and neuroinflammation, though its molecular mechanisms were not fully understood.
- This study found that reducing MANF expression increased inflammation (TNF-α), while exogenous MANF promoted autophagy, reduced α-synuclein levels, and inhibited neuroinflammation, suggesting that MANF could be a therapeutic target for PD through its role in autophagy.
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