Many pathogenic microorganisms have been demonstrated in atherosclerotic plaques 
and in cerebral plaques in dementia. Hyperhomocysteinemia, which is a risk 
factor for atherosclerosis and dementia, is caused by dysregulation of 
methionine metabolism secondary to deficiency of the allosteric regulator, 
adenosyl methionine. Deficiency of adenosyl methionine results from increased 
polyamine biosynthesis by infected host cells, causing increased activity of 
ornithine decarboxylase, decreased nitric oxide and peroxynitrate formation and 
impaired immune reactions. The down-regulation of oxidative phosphorylation that 
is observed in aging and dementia is attributed to deficiency of thioretinaco 
ozonide oxygen complexed with nicotinamide adenine dinucleotide and phosphate, 
which catalyzes oxidative phosphorylation. Adenosyl methionine biosynthesis is 
dependent upon thioretinaco ozonide and adenosine triphosphate (ATP), and the 
deficiency of adenosyl methionine and impaired immune function in aging are 
attributed to depletion of thioretinaco ozonide from mitochondrial membranes. 
Allyl sulfides and furanonaphthoquinones protect against oxidative stress and 
apoptosis by increasing the endogenous production of hydrogen sulfide and by 
inhibiting electron transfer to the active site of oxidative phosphorylation. 
Diallyl trisulfide and napabucasin inhibit the signaling by the signal 
transducer and activator of transcription 3 (Stat3), potentially enhancing 
immune function by effects on T helper lymphocytes and promotion of apoptosis. 
Homocysteine promotes endothelial dysfunction and apoptosis by the unfolded 
protein response and endoplasmic reticulum stress through activation of the 
N-methyl D-aspartate (NMDA) receptor, causing oxidative stress, calcium influx, 
apoptosis and endothelial dysfunction. The prevention of atherosclerosis and 
dementia may be accomplished by a proposed nutritional metabolic 
homocysteine-lowering protocol which enhances immunity and corrects the altered 
oxidative metabolism in atherosclerosis and dementia.