“Cerebrovascular insulin receptors are defective in Alzheimer’s disease”

1. Cerebrovascular: brain and blood vessels

2. “Insulin” is needed to bring sugar into a cell. Sugar is needed for energy for the cell. Without insulin the sugar stays outside of the cell in the blood. A glucose/sugar test for diabetics measures how much sugar is in the blood. Regular sugar levels are between 90-120.

3. Receptor: a docking port on the outside of a cell. A molecule docks on the receptor, and a variety of things can happen afterwards. In this case sugar is simply brought into the cell.

4. Blood Brain Barrier: The brain has a “border wall” so to say. It is highly selective of what it allows into the brain. In the article it explains that insulin is created in the pancreas which isn’t in the brain. Insulin transport across the blood brain barrier is low in Alzheimer’s patients, meaning that the brain isn’t getting the energy it needs for various functions namely, I suppose, to contribute to a reaction that stops the buildup of amyloid plaques on the brain, which are highly associated with Alzheimer’s.

5. Amyloid plaques (not mentioned in the article but I’ll write what I’ve studied about Alzheimer’s and the brain in general). Cells have a internal highway called microtubules which serve a variety of functions outside of the one relevant to this discussion. In nerve cells, neurotransmitters like dopamine, serotonin, noradrenaline, etc travel across microtubules (roughly) from one nerve to the other.

Amyloid are protein fragments that are naturally made in the body. Beta amyloids are the unfinished versions of the protein fragments. An accumulation of beta amyloid are called Amyloid plaques which play a role in destroying the microtubule highway up. This in turn prevents neurotransmitters from traveling across a cell.

5. (This is a very rough explanation of something that is way more complex, just trying to keep it as simple as possible) I’m assuming that since the brain isn’t receiving enough insulin from the pancreas, that the docking mechanism on the blood brain barrier isn’t taking sugar into the brain. This in turn is limiting the brain’s ability to catalyze the amyloid protein to completion and leaving behind the unfinished beta amyloid version, which forms a complex with (tau based) microtubules, triggering a disassembly of the highway. This makes it almost impossible for nutrients to travel across the cell and leads to “impaired long term potentiation,” leading to massive NEURON DEATH which is typical of AD brain.