response to amyloid-beta

Definition

Target type: biologicalprocess

Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a amyloid-beta stimulus. [GO_REF:0000071, GOC:TermGenie, PMID:23555824]

Response to amyloid-beta is a complex biological process involving multiple cellular pathways and molecular mechanisms. It is initiated by the accumulation of amyloid-beta (Aβ) peptides, which are naturally occurring fragments of the amyloid precursor protein (APP). Aβ aggregation leads to the formation of toxic oligomers and fibrils that disrupt neuronal function and trigger a cascade of events.

The first stage involves the recognition and binding of Aβ by cellular receptors, such as Toll-like receptors (TLRs) and scavenger receptors. This binding activates downstream signaling pathways, leading to the production of inflammatory mediators, including cytokines (e.g., TNF-α, IL-1β) and chemokines (e.g., MCP-1). These mediators contribute to the recruitment of immune cells, such as microglia and astrocytes, to the site of Aβ accumulation.

Microglia, the resident immune cells of the brain, play a crucial role in the response to Aβ. Upon activation, they engulf and degrade Aβ through phagocytosis. However, prolonged Aβ exposure can lead to microglial dysfunction, resulting in chronic inflammation and neuronal damage. Astrocytes, another type of glial cell, also contribute to the response by releasing neurotrophic factors that support neuronal survival and by forming a glial scar around Aβ deposits.

In addition to inflammation, Aβ accumulation triggers other cellular processes, including oxidative stress, mitochondrial dysfunction, and apoptosis. Oxidative stress is caused by the generation of reactive oxygen species (ROS) that damage cellular components. Mitochondrial dysfunction leads to energy deficits and increased ROS production. Apoptosis, or programmed cell death, is a process that eliminates damaged cells.

The response to Aβ is highly complex and can vary depending on the genetic background, age, and lifestyle of the individual. While the immune system is essential for clearing Aβ and protecting against neuronal damage, it can also contribute to the pathology of Alzheimer's disease by promoting chronic inflammation. Understanding the intricate interplay between Aβ and the cellular response is crucial for developing effective therapies for Alzheimer's disease.

Overall, the response to amyloid-beta is a multifaceted process involving the activation of immune cells, the production of inflammatory mediators, and the induction of cellular stress responses. It is a key determinant of the progression of Alzheimer's disease and a promising target for therapeutic interventions.'
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Proteins (14)

Compounds (625)