Figure 1.

Hypothetical working model.

Under non pathological conditions, a satiety hormone is triggering the release of rod-derived cone viability factor 2 (RdCVF2) from the area postrema to the 4th ventricle. RdCVF2 circulates in the cerebrospinal fluid and reach its cell surface receptor on hippocampal pyramidal neurons increasing glucose uptake via GLUT4. Aerobic glycolysis participates in the membrane surface increase to form new dendritic spines. Metabolism of this glucose by the pentose phosphate pathway (PPP) increases the redox power of thioredoxin, such as RdCVF2L that reduces TAU aggregation resulting from increase oxidative stress during aging.