{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T20:43:06Z","timestamp":1790023386863,"version":"4.0.1"},"reference-count":252,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2019,9,18]],"date-time":"2019-09-18T00:00:00Z","timestamp":1568764800000},"content-version":"vor","delay-in-days":20,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Fondazione Dieta Mediterranea"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Alzheimer\u2019s disease is associated with cerebral accumulation of amyloid-\u03b2 peptide and hyperphosphorylated tau. In the past 28 years, huge efforts have been made in attempting to treat the disease by reducing brain accumulation of amyloid-\u03b2 in patients with Alzheimer\u2019s disease, with no success. While anti-amyloid-\u03b2 therapies continue to be tested in prodromal patients with Alzheimer\u2019s disease and in subjects at risk of developing Alzheimer\u2019s disease, there is an urgent need to provide therapeutic support to patients with established Alzheimer\u2019s disease for whom current symptomatic treatment (acetylcholinesterase inhibitors and N-methyl d-aspartate antagonist) provide limited help. The possibility of an infectious aetiology for Alzheimer\u2019s disease has been repeatedly postulated over the past three decades. Infiltration of the brain by pathogens may act as a trigger or co-factor for Alzheimer\u2019s disease, with Herpes simplex virus type 1, Chlamydia pneumoniae, and Porphyromonas gingivalis being most frequently implicated. These pathogens may directly cross a weakened blood\u2013brain barrier, reach the CNS and cause neurological damage by eliciting neuroinflammation. Alternatively, pathogens may cross a weakened intestinal barrier, reach vascular circulation and then cross blood\u2013brain barrier or cause low grade chronic inflammation and subsequent neuroinflammation from the periphery. The gut microbiota comprises a complex community of microorganisms. Increased permeability of the gut and blood\u2013brain barrier induced by microbiota dysbiosis may impact Alzheimer\u2019s disease pathogenesis. Inflammatory microorganisms in gut microbiota are associated with peripheral inflammation and brain amyloid-\u03b2 deposition in subjects with cognitive impairment. Oral microbiota may also influence Alzheimer\u2019s disease risk through circulatory or neural access to the brain. At least two possibilities can be envisaged to explain the association of suspected pathogens and Alzheimer\u2019s disease. One is that patients with Alzheimer\u2019s disease are particularly prone to microbial infections. The other is that microbial infection is a contributing cause of Alzheimer\u2019s disease. Therapeutic trials with antivirals and\/or antibacterials could resolve this dilemma. Indeed, antiviral agents are being tested in patients with Alzheimer\u2019s disease in double-blind placebo-controlled studies. Although combined antibiotic therapy was found to be effective in animal models of Alzheimer\u2019s disease, antibacterial drugs are not being widely investigated in patients with Alzheimer\u2019s disease. This is because it is not clear which bacterial populations in the gut of patients with Alzheimer\u2019s disease are overexpressed and if safe, selective antibacterials are available for them. On the other hand, a bacterial protease inhibitor targeting P. gingivalis toxins is now being tested in patients with Alzheimer\u2019s disease. Clinical studies are needed to test if countering bacterial infection may be beneficial in patients with established Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.1093\/brain\/awz244","type":"journal-article","created":{"date-parts":[[2019,7,25]],"date-time":"2019-07-25T19:10:13Z","timestamp":1564081813000},"source":"Crossref","is-referenced-by-count":60,"title":["Time to test antibacterial therapy in Alzheimer\u2019s disease"],"prefix":"10.1093","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7220-0656","authenticated-orcid":false,"given":"Francesco","family":"Panza","sequence":"first","affiliation":[{"name":"Unit of Epidemiological Research on Aging, National Institute of Gastroenterology \u2018Saverio de Bellis\u2019, Research Hospital, Castellana Grotte, Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madia","family":"Lozupone","sequence":"additional","affiliation":[{"name":"Unit of Epidemiological Research on Aging, National Institute of Gastroenterology \u2018Saverio de Bellis\u2019, Research Hospital, Castellana Grotte, Bari, Italy"},{"name":"Neurodegenerative Disease Unit, Department of Basic Medicine, Neuroscience, and Sense Organs, University of Bari Aldo Moro, Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vincenzo","family":"Solfrizzi","sequence":"additional","affiliation":[{"name":"\u2018C. Frugoni\u2019 Internal and Geriatric Medicine and Memory Unit, University of Bari Aldo Moro, Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Watling","sequence":"additional","affiliation":[{"name":"Department of Research and Development, Chiesi Farmaceutici, Parma, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruno P","family":"Imbimbo","sequence":"additional","affiliation":[{"name":"Department of Research and Development, Chiesi Farmaceutici, Parma, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,8,29]]},"reference":[{"key":"2019091810412661800_awz244-B1","doi-asserted-by":"crossref","first-page":"254","DOI":"10.1016\/j.bbi.2016.07.153","article-title":"High avidity HSV-1 antibodies correlate with absence of amnestic Mild Cognitive Impairment conversion to Alzheimer\u2019s 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