Genetic and sporadic cases of Alzheimer’s disease (AD) are known, but the aetiology is mostly unknown. We wanted to look for metabolic deviations of low MW compounds that may point to key pathways involved in the disease aetiology. In first morning urines Neopterin, Biopterin (Immunology related), 8-oxo-deoxyguanosine and 8-oxo-guanosine (oxidative stress), porphyrin profiles (metal toxicity) and peptide like compounds separated on HPLC, were measured. All measures were related to Creatinin. All the patients showed cellular immune activation. 70% showed signs of severe inflammatory cyto-plasmic RNA oxidation, with 30% showed moderate increase. DNA damage measured as 8-oxo-deoxyguanosine. The AD patient showed peptide increases. Porphyrin profiles showed statistically significant increase in coproporphyrins I and III.  We may conclude that cellular immune activation and a large cytoplasmic inflammatory process are found in AD. The process may take place outside the CNS. Increase in peptides point to a decrease in their normal metabolism. The porphyrin profiles indicate involvement of possibly Aluminum. Apparently the greatest changes are in markers of oxidative stress.