The brain is a privileged organ. Even in times of hypoxia, it tries to remain protected. An example is the "diving reflex" and mechanisms of shock where blood is cut from the periphery and shunted to the CNS. CNS has the smallest vessels know to exist. Especially in noble aras such as the hypocampus, visual and motor cortex. This can to some extent compensate for low carring capacity.
Now, as oxygenation decreases due to lack of carrying capacity, the oxygen dessaturation curve will attempt to adjust but this is not effective. It will come a time where O2 saturation in the brain parenchyma will become insufficient and this is reflected in dizziness, visual changes, confusion etc, as the function of the neural cells responsible for these is affected. Increased perfusion, is attempted by increased heart rate (anemia causes tachycardia) but this is not sufficient. Eventually severe anoxia will result in acidosis and cell death. One intersting issue you may want to look up is that different types of hemoblobin are more effective at transporting oxygen. Fetal hemoglobin, Hgb -F is manyfold more efficient in delivering the O2 . Remember that in utero, fetal O2 saturarion is only 23 to 30 %! Nevertheless fetuses devellop and function normally in this relatively hypoxic environment. Normal O2 Saturartion in adults is >90% at the extremities (pulse oxymeter). Just think that if O2 saturation is 92% at the tip of one's finger it is much greate in the CNS. I hope this helps.