Neuronal Apoptosis
Programmed neuron death. Unlike muscle, these cells are largely not replaced, so this process is where a reversible effect becomes a permanent one. Everything protective in this module ultimately resolves to whether it raises or lowers this.
Relationships
5 connectionsNeuronal Apoptosis reduces risk of
Cognitive Function
Memory, focus and processing speed. It is the endpoint the nootropic peptides claim, and the one that is hardest to measure honestly outside a controlled trial.
Cortical Thickness
How thick the outer layer of the brain is, measured on MRI. It thins with normal ageing and faster in several dependencies. In steroid users the thinning is regional, and it is concentrated in exactly the areas that handle inhibition.
Mitochondrial Calcium Buffering
How much calcium a neuron's mitochondria can absorb before the cell dies. This is the single most underrated number in the whole estrogen argument: estradiol does not stop calcium entering the neuron, it raises the amount the neuron can survive.
Neuronal Apoptosis stimulates
Excitotoxic Injury
Death by over-stimulation. Glutamate opens calcium channels, calcium floods in past what the mitochondria can hold, and the cell triggers its own destruction. It is the final common path for a large share of neuronal death, and it is the exact process estrogen defends against.
Neuroinflammation
Immune activation inside brain tissue. Short bursts are protective. Sustained activation is not, and it limits the very functions the immune cells were maintaining. Estrogen is one of the main brakes on it, which is the mechanistic core of why crashing estrogen has a cost.
Beyond this page
Neuronal Apoptosis also connects to 4 entries in the applied modules, covering supplements, compounds, hormones and food sources. Those carry the mechanism and the evidence tier behind each link, and they are part of client coaching.
Get your free assessment