{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T17:09:40Z","timestamp":1777396180743,"version":"3.51.4"},"reference-count":109,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2022,11,22]],"date-time":"2022-11-22T00:00:00Z","timestamp":1669075200000},"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":[[2022,11,22]]},"abstract":"<jats:p>Although the cause(s) of Alzheimer\u2019s disease in the majority of cases remains elusive, it has long been associated with hypertension. In animal models of the disease, hypertension has been shown to exacerbate Alzheimer-like pathology and behavior, while in humans, hypertension during mid-life increases the risk of developing the disease later in life. Unfortunately, once individuals are diagnosed with the disease, there are few therapeutic options available. There is neither an effective symptomatic treatment, one that treats the debilitating cognitive and memory deficits, nor, more importantly, a neuroprotective treatment, one that stops the relentless progression of the pathology. Further, there is no specific preventative treatment that offsets the onset of the disease. A key factor or clue in this quest for an effective preventative and therapeutic treatment may lie in the contribution of hypertension to the disease. In this review, we explore the idea that photobiomodulation, the application of specific wavelengths of light onto body tissues, can reduce the neuropathology and behavioral deficits in Alzheimer\u2019s disease by controlling hypertension. We suggest that treatment with photobiomodulation can be an effective preventative and therapeutic option for this neurodegenerative disease.<\/jats:p>","DOI":"10.3233\/jad-220632","type":"journal-article","created":{"date-parts":[[2022,9,30]],"date-time":"2022-09-30T12:35:08Z","timestamp":1664541308000},"page":"1045-1055","source":"Crossref","is-referenced-by-count":22,"title":["Photobiomodulation for Hypertension and Alzheimer\u2019s Disease"],"prefix":"10.1177","volume":"90","author":[{"given":"Audrey","family":"Valverde","sequence":"first","affiliation":[{"name":"Universit\u00e9 Grenoble Alpes, Fonds de dotation Clinatec, Grenoble, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John","family":"Mitrofanis","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Grenoble Alpes, Fonds de dotation Clinatec, Grenoble, France"},{"name":"Institute of Ophthalmology, University College London, London, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-220632_ref1","doi-asserted-by":"crossref","first-page":"1019","DOI":"10.1016\/S0140-6736(10)61349-9","article-title":"Alzheimer\u2019s disease","volume":"377","author":"Ballard","year":"2011","journal-title":"Lancet"},{"key":"10.3233\/JAD-220632_ref2","doi-asserted-by":"crossref","first-page":"595","DOI":"10.15252\/emmm.201606210","article-title":"The amyloid hypothesis of Alzheimer\u2019s disease at 25 years","volume":"8","author":"Selkoe","year":"2016","journal-title":"EMBO Mol Med"},{"key":"10.3233\/JAD-220632_ref3","doi-asserted-by":"crossref","first-page":"95","DOI":"10.1016\/j.mad.2016.05.005","article-title":"Molecular pathophysiology of impaired glucose metabolism, mitochondrial dysfunction, and oxidative DNA damage in Alzheimer\u2019s disease brain","volume":"161","author":"Abolhassani","year":"2017","journal-title":"Mech Ageing Dev"},{"key":"10.3233\/JAD-220632_ref4","doi-asserted-by":"crossref","first-page":"109","DOI":"10.1038\/nrn3887","article-title":"Spreading of pathology in neurodegenerative diseases: A focus on human studies","volume":"16","author":"Brettschneider","year":"2015","journal-title":"Nat Rev Neurosci"},{"key":"10.3233\/JAD-220632_ref5","doi-asserted-by":"crossref","first-page":"1255555","DOI":"10.1126\/science.1255555","article-title":"Alzheimer\u2019s and Parkinson\u2019s diseases: The prion concept in relation to assembled A\u03b2, tau, and \u03b1-synuclein","volume":"349","author":"Goedert","year":"2015","journal-title":"Science"},{"issue":"Suppl 2","key":"10.3233\/JAD-220632_ref6","doi-asserted-by":"crossref","first-page":"237","DOI":"10.1111\/jnc.13632","article-title":"The amyloid cascade hypothesis: Are we poised for success or failure?","volume":"139","author":"Karran","year":"2016","journal-title":"J Neurochem"},{"key":"10.3233\/JAD-220632_ref7","doi-asserted-by":"crossref","first-page":"505","DOI":"10.1016\/S0140-6736(15)01124-1","article-title":"Alzheimer\u2019s disease","volume":"388","author":"Scheltens","year":"2016","journal-title":"Lancet"},{"key":"10.3233\/JAD-220632_ref8","first-page":"239","article-title":"Cerebrovascular disease and the pathophysiology of Alzheimer\u2019s disease. 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