Alzheimer's Disease: Functional Therapeutics in Neurodegenerative Disease
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Alzheimer's Disease: Functional Therapeutics in Neurodegenerative Disease
David Perlmutter, M.D.
www.pcrm.org

Functional Intervention

The energy-linked excitotoxic model described above reveals multiple targets of susceptibility whereby compromised function can begin a progressive, feed-forward and thus self-perpetuating cascade ultimately culminating in neuronal death. These include excessive glutamate leading to excessive NMDA receptor stimulation (as noted in cerebral ischemia and amyotrophic lateral sclerosis); enhanced NMDA receptor sensitivity to glutamate as a consequence of altered electro-chemical gradient due to decreased mitochondrial ATP production (as noted in idiopathic Parkinson’s disease, MPTP-induced Parkinsonism, Huntington’s chorea, Alzheimer’s disease, and various inherited mitochondropathies); formation of NMDA receptor antibodies allowing persistent cellular inflow of calcium (noted in amyotrophic lateral sclerosis); enhanced nitric oxide production (as noted in Parkinson’s disease, Alzheimer’s disease, animal models, multiple sclerosis animal models, and ischemic stroke); deficiencies of small molecule antioxidants and antioxidant enzymes (Huntington’s chorea, Alzheimer’s disease, amyotrophic lateral sclerosis, and Parkinson’s disease); and deficiencies of xenobiotic metabolism allowing accumulation of neuro-toxic intermediates (amyotrophic lateral sclerosis, Alzheimer’s disease, and Parkinson’s disease).

References

Go on to: Inhibition of Glutamate Release/NMDA Stimulation
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