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Alzheimer’s Disease: The Great Morbidity of the 21st Century

Neuroangiogenesis (NAG) provides a vascular basis for understanding Alzheimer’s disease, senile dementias and cognitive decline with aging

Charles T. Ambrose

Neuroangiogenesis Hypothesis

The neuroangiogenic (NAG) hypothesis proposes that Alzheimer’s disease and the various dementias of the aged have in common a reduced microcirculation in key regions of the brain due to a waning number of cerebral capillaries with aging. The level of neuroangiogenic factors there is less than that needed to maintain a full complement of functional capillaries.

My interest in impaired cognition with aging stemmed from an earlier fascination with the localized motor skills highly developed in intensely trained musicians. In a 2010 article in American Scientist I proposed that the remarkable finger/hand/foot dexterity displayed by concert pianists is due not only to augmented synaptic connections in their primary motor cortex but also to an increased local capillary density (CD)—initiated and maintained there by continuing angiogenesis. Considerable data from the nonmusical neurological literature support this idea. I reasoned that if an increased local CD could account for remarkable motor skills of pianists, a decreased CD elsewhere in the brain might cause impairment—for example, the declining cognition of many aged persons.

This essay continues in two sections: The first concerns cerebral capillary density (CCD), whereas the second treats the formation and maintenance of these capillaries by neuroangiogenesis (NAG). In both sections the brain is analyzed during its three periods of life (during postnatal development, maturity and old age) and in cases of senile dementias (mainly AD). In each section, animal findings are cited before comparable ones in people. Next are summarized studies on brain-injured animals treated with angiogenic factors. The essay concludes with six approaches for administering such factors to persons with senile dementias.

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