Amyloid-ß (Aβ) is a peptide that has been studied extensively in the context of Alzheimer’s disease. Aβ is produced by misfolding of amyloid precursor protein (APP), and accumulates as insoluble aggregates called amyloid plaques. These plaques are considered to be one of the hallmarks of Alzheimer’s Disease, and have been found in many other neurological diseases such as Parkinson’s, Creutzfeldt-Jakob, Down Syndrome, and stroke.
Aβ can be divided into two different forms: Aβ40 and Aβ42. The former consists of 40 amino acids while the latter consists of 42 amino acids; both differ slightly in their sequence structure though they have similar functions. There is evidence suggesting that Aβ42 has a higher propensity for aggregation than its shorter counterpart; this has led to the hypothesis that excessive accumulation of Aβ42 could play a role in memory impairment associated with Alzheimer’s disease pathology.
The mechanisms involved in formation and clearance pathways for these aggregates are still under active investigation; however, it seems likely that autophagy plays an important role here by promoting removal or degradation via lysosomes before plaque formation occurs . Additionally, recent studies suggest that APP processing may also modulate expression levels or activities related to factors such as endocytosis which could affect how much soluble or insoluble material is available for aggregation processes to occur.
Yan et al., 2019 Arancio et al., 2018
In addition to being linked with neurodegenerative conditions like Alzheimer’s disease, accumulating research suggests there may exist more subtle roles for amyloid-ß outside neuronal cells too – specifically within immune cell populations where it appears to act proinflammatory mediator. Recent work has further suggested some involvement between IL-17 signaling pathways & production/secretion patterns from monocytes when exposed exogenous sources – possibly indicating some modulation on regulatory T-cell populations during infection responses. Although speculative at present time it would appear clear there exists potential implications regarding immunomodulatory effects which warrants further exploration into possible therapeutic strategies targeting specific interactions between Aß & inflammatory cytokines going forward .
Kim et al., 2016 Zhang et al., 2017