{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T17:05:35Z","timestamp":1777395935407,"version":"3.51.4"},"reference-count":35,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2021,10,26]],"date-time":"2021-10-26T00:00:00Z","timestamp":1635206400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2021,10,26]]},"abstract":"<jats:p>Utilizing the pathology and microbiology found in tissue from patients with documented Alzheimer\u2019s disease (AD), the pathogenesis of this fateful disorder has been made clear. Borrelia burgdorferi and Treponema denticola spirochetes enter the brain, mostly via neuronal pathways and the entorhinal circulation. These organisms easily pass through the blood-brain barrier and have an affinity for neural tissue. Once in the brain, the spirochetes make intra- and extracellular biofilms, and it is the biofilms that create the pathology. Specifically, it is the intracellular biofilms that are ultimately responsible for neurofibrillary tangles and dendritic disintegration. The extracellular biofilms are responsible for the inflammation that initially is generated by the first responder, Toll-like receptor 2. The hypothesis that arises from this work is two-pronged: one is related to prevention; the other to treatment. Regarding prevention, it is very likely possible that AD could be prevented by periodic administration of penicillin (PCN), which would kill the spirochetes before they made biofilms; this would prevent the disease and would not allow any of the above deleterious changes generated by the biofilms to occur. As regards treatment, it may be possible to slow or prevent further decline in early AD by administration of PCN together with a biofilm disperser. The disperser would disrupt the biofilm coating and enable the PCN to kill the spirochetes. This protocol could be administered in a trial with the control arm utilizing the current treatment. The progress of the treatment could be evaluated by one of the current blood tests that is semi-quantitative. The specific protocols are listed.<\/jats:p>","DOI":"10.3233\/jad-210429","type":"journal-article","created":{"date-parts":[[2021,9,14]],"date-time":"2021-09-14T11:04:33Z","timestamp":1631617473000},"page":"61-67","source":"Crossref","is-referenced-by-count":10,"title":["A Novel Approach to the Treatment and Prevention of Alzheimer\u2019s Disease Based on the Pathology and Microbiology"],"prefix":"10.1177","volume":"84","author":[{"given":"Herbert B.","family":"Allen","sequence":"first","affiliation":[{"name":"Department of Dermatology, Drexel University College of Medicine, Philadelphia, PA, USA"},{"name":"Dermatology, Eastern Virginia Medical School, Norfolk, VA, USA"},{"name":"Geriatrics and Gerontology, Rowan School of Osteopathic Medicine, Stratford, NJ, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-210429_ref1","doi-asserted-by":"crossref","first-page":"97","DOI":"10.3390\/biomedicines7040097","article-title":"Reasons for failed trials of disease-modifying treatments for Alzheimer disease and their contribution in recent research","volume":"7","author":"Yiannopolou","year":"2019","journal-title":"Biomedicines"},{"key":"10.3233\/JAD-210429_ref2","doi-asserted-by":"crossref","first-page":"1539","DOI":"10.1007\/s12272-010-1006-7","article-title":"Inflammation and Alzheimer\u2019s disease","volume":"33","author":"Lee","year":"2010","journal-title":"Arch Pharm Res"},{"key":"10.3233\/JAD-210429_ref3","doi-asserted-by":"crossref","first-page":"90","DOI":"10.1186\/1742-2094-8-90","article-title":"Alzheimer\u2019s disease - a neurospirochetosis. 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