Publications by authors named "Priscila Baltazar Goncalves"

Article Synopsis
  • - Alzheimer's disease (AD) is a serious global health challenge with no cure, marked by brain degeneration and cognitive decline; current treatments mainly manage symptoms rather than modify the disease itself.
  • - The accumulation of amyloid-β (Aβ) peptides plays a key role in AD pathology, and there's a shift in focus from targeting mature amyloid fibrils to addressing more toxic soluble Aβ oligomers that damage nerve cells and synapses.
  • - Natural products show promise in combating Aβ oligomer neurotoxicity through various strategies, suggesting they could lead to new, effective treatments for AD by understanding how they influence Aβ oligomer behavior in different experimental settings.
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Oligomeric species of amyloid β peptide (Aβ) are pivotal in Alzheimer's disease (AD) pathogenesis, making them valuable therapeutic targets. Currently, there is no cure or preventive therapy available for AD, with only a few therapeutics offering temporary alleviation of symptoms. Natural products (NPs) are now considered promising anti-amyloid agents.

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The misfolding and aggregation of the presynaptic protein α-synuclein (α-syn) is a pathological hallmark of Parkinson's disease (PD). Targeting α-syn has emerged as a promising therapeutic strategy for PD. Emerging evidence supports a dual action of epigallocatechin-3-gallate (EGCG) against amyloid neurotoxicity.

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The potential to treat neurodegenerative diseases (NDs) of the major bioactive compound of green tea, epigallocatechin-3-gallate (EGCG), is well documented. Numerous findings now suggest that EGCG targets protein misfolding and aggregation, a common cause and pathological mechanism in many NDs. Several studies have shown that EGCG interacts with misfolded proteins such as amyloid beta-peptide (Aβ), linked to Alzheimer's disease (AD), and α-synuclein, linked to Parkinson's disease (PD).

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Chronic Obstructive Pulmonary Disease (COPD) is a major global health problem. Among other conditions, it has been associated with chronic airway and lung parenchyma inflammation. At present, the available therapies are not capable of reducing the progression or suppressing inflammation associated to COPD.

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