The Hidden Powerhouse: How Tiny Mitochondria Fuel Alzheimer's

Alzheimer's disease is a complex puzzle. One key piece? Tiny powerhouses in our cells called mitochondria. These little guys usually help cells stay alive and healthy. But in Alzheimer's, they're not working right. Why? Because calcium, a crucial messenger in cells, is out of balance. Calcium is like a traffic cop. It directs important processes in brain cells. But when too much calcium piles up in mitochondria, trouble starts. The mitochondria can't make enough energy. They also start creating harmful stuff called reactive oxygen species. This leads to brain cell damage and, eventually, cognitive decline. Two bad actors in Alzheimer's, amyloid-β (Aβ) peptides and neurofibrillary tangles (NFTs), make this problem worse. They mess up calcium regulation even more. Plus, some genes linked to Alzheimer's risk, like ApoE4, also play a role in calcium imbalance. Mitochondria have special gates for calcium, like the MCU and NCLX. When these gates aren't working right, it's like a traffic jam. Calcium can't move properly. This makes the mitochondria's job even harder. Understanding this process is crucial. If we can find ways to control calcium levels in mitochondria, we might be able to slow down or even stop Alzheimer's. This could also help with other brain diseases. But it's not just about Alzheimer's. Mitochondrial calcium dysregulation is linked to many health issues. So, solving this puzzle could have big implications.