Abstract
Alzheimer's disease (AD) is associated with considerably decreased cerebral blood flow (CBF) thought to be secondary, since dead neurons do not need oxygen and glucose. This view, however, needs to be critically re-examined.
The role of CBF in AD was submitted to a thorough analysis, raising the question: “Is there really a lack of demand in the presence of undisturbed blood supply?”
CBF decline is present in AD while the number of affected CNS systems is still quite small. The step-by-step evolution of AD mirrors a brain that progressively becomes ischemic. Areas related to memory function (hippocampus, temporal lobe cortex and vicinity) are bound to suffer first because of their particularly vulnerable blood supply.
This is the scenario of a disorder caused by primary and not by secondary CBF deficiency—a deficiency perhaps attributable to the upright gait of homo sapiens. This new approach also opens new avenues for treatment and prevention, which will be briefly discussed.
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