Membrane-enclosed organelles are a crucial characteristic of eukaryotic cells, facilitating the compartmentalization of specific biochemical reactions and processes.
While traditional textbooks still depict organelles as isolated entities, it is now recognized that all organelles maintain continuous communication through membrane contact sites.
These membrane structures create an optimal environment for cells to rapidly respond to various physiological or pathological cues.
Due to its extensive membrane network, the endoplasmic reticulum (ER) establishes membrane contact sites with various organelles to maintain communication, including mitochondria, Golgi apparatus, endosomes and peroxisomes.
Among these, the most extensively studied are the sites formed between the ER membranes and mitochondria, known as MAMs.
The formation of these domains plays a role in regulating various crucial biological processes, such as lipid synthesis, calcium balance, inflammation, mitochondrial quality control, and even cell death, by selectively recruiting and activating specific lipids and proteins.
The abnormal increase in MAMs discovered in the postmortem brains of AD patients has sparked significant interest in its role in AD.
Subsequent research has revealed that changes in MAMs occur early in the progression of AD and are implicated in several crucial early pathological events associated with the disease.
Additionally, abnormalities in MAMs play a role in triggering mitochondrial dysfunction in AD by impacting mitochondrial quality control.
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