{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T14:28:29Z","timestamp":1785421709257,"version":"3.56.0"},"reference-count":35,"publisher":"MDPI AG","issue":"7","license":[{"start":{"date-parts":[[2026,7,18]],"date-time":"2026-07-18T00:00:00Z","timestamp":1784332800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000090","name":"Congressionally Directed Medical Research Programs","doi-asserted-by":"publisher","award":["W81XWH-20-1-0479"],"award-info":[{"award-number":["W81XWH-20-1-0479"]}],"id":[{"id":"10.13039\/100000090","id-type":"DOI","asserted-by":"publisher"}]},{"award":["W81XWH-20-1-0479"],"award-info":[{"award-number":["W81XWH-20-1-0479"]}],"id":[{"id":"https:\/\/ror.org\/03g2zjp07","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Brain Sciences"],"abstract":"<jats:p>Background\/Objectives: Alzheimer\u2019s Disease (AD) and vascular dementia contribute up to ~75% of dementia cases, as determined via autopsy. AD arises in part due to the buildup of aberrant proteins (amyloid beta (A\u03b2) and Tau); vascular dementia is caused by reduced cerebral blood flow. Each dementia mechanisms damages brain. Bobola et al. found that their low-intensity focused ultrasound (FUS) protocol applied to the brains of the 5XFAD mouse model of AD reduced A\u03b2 by 50% through activation of microglia. Eguchi et al. found that their own FUS protocol applied to the brains of the same mouse model reduced A\u03b2 by 15% and increased cerebral blood flow by 50% through an increase in endothelial nitric oxide synthase (eNOS). Here, we sought to test a combined version of those two FUS protocols, expecting both a decrease in A\u03b2 burden and an increase in eNOS. Methods: Using a diagnostic ultrasound probe, we applied our combined FUS protocol primarily to the left hippocampus of anesthetized 5XFAD mice, for an hour a day, for three days for younger mice and for five days for older mice. On day three or five, respectively, we harvested their brains and performed histological analysis to assess A\u03b2 burden, microglial activation and their co-localization with A\u03b2, as well as the burden of eNOS within neuronal nuclei (here called intra-neuronal eNOS) and outside of neurons. Results: Relative to untreated mice, the treated younger mice had more activated microglia co-localized with A\u03b2 and reduced A\u03b2 burden for large plaques, as well as no change in each measure of eNOS. In contrast, the treated older AD mice had no change in activated microglia co-localized with A\u03b2, and no change in A\u03b2 burden. However, relative to untreated older AD mice, FUS decreased total and extra-neuronal eNOS and increased intra-neuronal eNOS. Conclusions: The ability of our FUS protocol to reduce A\u03b2 burden and alter the eNOS distribution depends critically upon the age of the AD mice (more A\u03b2 plaques for a comparable number of microglia for older mice relative to younger mice) and duration of the treatment. The observed decrease in extra-neuronal eNOS distribution in older AD mice caused by FUS raises the concern that our protocol may increase ischemia, while the increase in intra-neuronal eNOS may counteract that effect via protection of synaptic function. These findings also identify two candidate therapeutic windows for our FUS treatment protocol, each requiring more research before translation to humans. One window is early intervention to maximize A\u03b2 plaque removal via activation of microglia. The second is later intervention to protect synaptic function if it is possible to mitigate the potential ischemic risk caused by the differential effects of FUS on eNOS.<\/jats:p>","DOI":"10.3390\/brainsci16070757","type":"journal-article","created":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T10:44:02Z","timestamp":1784544242000},"page":"757","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Low-Intensity Focused Ultrasound Alters Alzheimer\u2019s Disease Pathology, In Vivo, as a Function of Ultrasound Dose and Age"],"prefix":"10.3390","volume":"16","author":[{"given":"Alissa","family":"Phutirat","sequence":"first","affiliation":[{"name":"Department of Neurological Surgery, University of Washington, Seattle, WA 98195, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kahte A.","family":"Culevski","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, University of Washington, Seattle, WA 98195, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah","family":"Mach","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, University of Washington, Seattle, WA 98195, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamie","family":"Kwon","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, University of Washington, Seattle, WA 98195, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-3600-9279","authenticated-orcid":false,"given":"Henry","family":"Tan","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, University of Washington, Seattle, WA 98195, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabe","family":"Koh","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, University of Washington, Seattle, WA 98195, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caren","family":"Marzban","sequence":"additional","affiliation":[{"name":"Applied Physics Laboratory, University of Washington, Seattle, WA 98195, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre D.","family":"Mourad","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, University of Washington, Seattle, WA 98195, USA"},{"name":"Division of Engineering and Mathematics, University of Washington, Bothell, WA 98011, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,7,18]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1774","DOI":"10.1111\/jgs.17345","article-title":"Impact of dementia: Health disparities, population trends, care interventions, and economic costs","volume":"69","author":"Aranda","year":"2021","journal-title":"J. Am. Geriatr. Soc."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"1791","DOI":"10.1212\/WNL.58.12.1791","article-title":"Phases of A\u0392-deposition in the human brain and its relevance for the development of AD","volume":"58","author":"Thal","year":"2002","journal-title":"Neurology"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/j.jalz.2011.10.007","article-title":"National Institute on Aging-Alzheimer\u2019s Association guidelines for the neuropathologic assessment of Alzheimer\u2019s disease","volume":"8","author":"Hyman","year":"2012","journal-title":"Alzheimer\u2019s Dement. J. Alzheimer\u2019s Assoc."},{"key":"ref_4","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1007\/s00401-011-0910-3","article-title":"National Institute on Aging-Alzheimer\u2019s Association guidelines for the neuropathologic assessment of Alzheimer\u2019s disease: A practical approach","volume":"123","author":"Montine","year":"2012","journal-title":"Acta Neuropathol."},{"key":"ref_5","doi-asserted-by":"crossref","first-page":"15056","DOI":"10.1038\/nrdp.2015.56","article-title":"Alzheimer\u2019s disease","volume":"1","author":"Masters","year":"2015","journal-title":"Nat. Rev. Dis. Prim."},{"key":"ref_6","doi-asserted-by":"crossref","first-page":"6","DOI":"10.1186\/s13073-023-01155-w","article-title":"The neuroimmune axis of Alzheimer\u2019s disease","volume":"15","author":"Jorfi","year":"2023","journal-title":"Genome Med."},{"key":"ref_7","doi-asserted-by":"crossref","first-page":"6893","DOI":"10.1523\/JNEUROSCI.4002-14.2015","article-title":"Nitric oxide signaling is recruited as a compensatory mechanism for sustaining synaptic plasticity in Alzheimer\u2019s disease mice","volume":"35","author":"Chakroborty","year":"2015","journal-title":"J. Neurosci. Off. J. Soc. Neurosci."},{"key":"ref_8","doi-asserted-by":"crossref","unstructured":"Yuste, J.E., Tarragon, E., Campuzano, C.M., and Ros-Bernal, F. (2015). Implications of glial nitric oxide in neurodegenerative diseases. Front. Cell. Neurosci., 9.","DOI":"10.3389\/fncel.2015.00322"},{"key":"ref_9","doi-asserted-by":"crossref","first-page":"13764","DOI":"10.1038\/s41598-019-50205-0","article-title":"Targeted metabolomic analysis of nitric oxide\/L-arginine pathway metabolites in dementia: Association with pathology, severity, and structural brain changes","volume":"9","author":"Fleszar","year":"2019","journal-title":"Sci. Rep."},{"key":"ref_10","doi-asserted-by":"crossref","first-page":"102203","DOI":"10.1016\/j.arr.2024.102203","article-title":"Comparative efficacy, tolerability and acceptability of donanemab, lecanemab, aducanumab and lithium on cognitive function in mild cognitive impairment and Alzheimer\u2019s disease: A systematic review and network meta-analysis","volume":"94","author":"Terao","year":"2024","journal-title":"Ageing Res. Rev."},{"key":"ref_11","doi-asserted-by":"crossref","first-page":"230","DOI":"10.1038\/nature20587","article-title":"Gamma frequency entrainment attenuates amyloid load and modifies microglia","volume":"540","author":"Iaccarino","year":"2016","journal-title":"Nature"},{"key":"ref_12","doi-asserted-by":"crossref","first-page":"256","DOI":"10.1016\/j.cell.2019.02.014","article-title":"Multi-sensory Gamma Stimulation Ameliorates Alzheimer\u2019s-Associated Pathology and Improves Cognition","volume":"177","author":"Martorell","year":"2019","journal-title":"Cell"},{"key":"ref_13","doi-asserted-by":"crossref","unstructured":"Chan, D., Suk, H.J., Jackson, B.L., Milman, N.P., Stark, D., Klerman, E.B., Kitchener, E., Fernandez Avalos, V.S., de Weck, G., and Banerjee, A. (2022). Gamma frequency sensory stimulation in mild probable Alzheimer\u2019s dementia patients: Results of feasibility and pilot studies. PLoS ONE, 17.","DOI":"10.1371\/journal.pone.0278412"},{"key":"ref_14","doi-asserted-by":"crossref","first-page":"278ra33","DOI":"10.1126\/scitranslmed.aaa2512","article-title":"Scanning ultrasound removes amyloid-\u03b2 and restores memory in an Alzheimer\u2019s disease mouse model","volume":"7","author":"Leinenga","year":"2015","journal-title":"Sci. Transl. Med."},{"key":"ref_15","doi-asserted-by":"crossref","first-page":"4102","DOI":"10.7150\/thno.79898","article-title":"Focused ultrasound mitigates pathology and improves spatial memory in Alzheimer\u2019s mice and patients","volume":"13","author":"Karakatsani","year":"2023","journal-title":"Theranostics"},{"key":"ref_16","doi-asserted-by":"crossref","first-page":"55","DOI":"10.1056\/NEJMoa2308719","article-title":"Ultrasound Blood-Brain Barrier Opening and Aducanumab in Alzheimer\u2019s Disease","volume":"390","author":"Rezai","year":"2024","journal-title":"N. Engl. J. Med."},{"key":"ref_17","doi-asserted-by":"crossref","first-page":"681","DOI":"10.1016\/j.mric.2024.03.001","article-title":"Focused Ultrasound for Neurodegenerative Diseases","volume":"32","author":"Mehta","year":"2024","journal-title":"Magn. Reson. Imaging Clin. N. Am."},{"key":"ref_18","doi-asserted-by":"crossref","first-page":"8","DOI":"10.1016\/j.brainresbull.2019.08.002","article-title":"Scanning ultrasound in the absence of blood-brain barrier opening is not sufficient to clear \u03b2-amyloid plaques in the APP23 mouse model of Alzheimer\u2019s disease","volume":"153","author":"Leinenga","year":"2019","journal-title":"Brain Res. Bull."},{"key":"ref_19","doi-asserted-by":"crossref","unstructured":"Balbi, M., Blackmore, D.G., Padmanabhan, P., and G\u00f6tz, J. (2022). Ultrasound-Mediated Bioeffects in Senescent Mice and Alzheimer\u2019s Mouse Models. Brain Sci., 12.","DOI":"10.3390\/brainsci12060775"},{"key":"ref_20","doi-asserted-by":"crossref","first-page":"374","DOI":"10.1016\/j.trci.2019.06.007","article-title":"Focused transcranial ultrasound for treatment of neurodegenerative dementia","volume":"5","author":"Nicodemus","year":"2019","journal-title":"Alzheimer\u2019s Dement. Transl. Res. Clin. Interv."},{"key":"ref_21","doi-asserted-by":"crossref","first-page":"1014","DOI":"10.1016\/j.brs.2020.03.016","article-title":"Transcranial focused ultrasound, pulsed at 40 Hz, activates microglia acutely and reduces A\u03b2 load chronically, as demonstrated in vivo","volume":"13","author":"Bobola","year":"2020","journal-title":"Brain Stimul."},{"key":"ref_22","doi-asserted-by":"crossref","first-page":"48","DOI":"10.1186\/s40035-021-00274-x","article-title":"Effects of transcranial ultrasound stimulation pulsed at 40 Hz on A\u03b2 plaques and brain rhythms in 5\u00d7FAD mice","volume":"10","author":"Park","year":"2021","journal-title":"Transl. Neurodegener."},{"key":"ref_23","doi-asserted-by":"crossref","first-page":"959","DOI":"10.1016\/j.brs.2018.05.012","article-title":"Whole-brain low-intensity pulsed ultrasound therapy markedly improves cognitive dysfunctions in mouse models of dementia-Crucial roles of endothelial nitric oxide synthase","volume":"11","author":"Eguchi","year":"2018","journal-title":"Brain Stimul."},{"key":"ref_24","doi-asserted-by":"crossref","unstructured":"Oblak, A.L., Lin, P.B., Kotredes, K.P., Pandey, R.S., Garceau, D., Williams, H.M., Uyar, A., O\u2019Rourke, R., O\u2019Rourke, S., and Ingraham, C. (2021). Comprehensive Evaluation of the 5XFAD Mouse Model for Preclinical Testing Applications: A MODEL-AD Study. Front. Aging Neurosci., 13.","DOI":"10.3389\/fnagi.2021.713726"},{"key":"ref_25","doi-asserted-by":"crossref","first-page":"114919","DOI":"10.1016\/j.bbr.2024.114919","article-title":"Age dependent path integration deficit in 5xFAD mice","volume":"463","author":"Mar","year":"2024","journal-title":"Behav. Brain Res."},{"key":"ref_26","first-page":"637","article-title":"Mouse models in aging research","volume":"Volume 3","author":"Fox","year":"2007","journal-title":"The Mouse in Biomedical Research"},{"key":"ref_27","doi-asserted-by":"crossref","first-page":"175","DOI":"10.3758\/BF03193146","article-title":"G*Power 3: A flexible statistical power analysis program for the social, behavioral, and biomedical sciences","volume":"39","author":"Faul","year":"2007","journal-title":"Behav. Res. Methods"},{"key":"ref_28","unstructured":"Devore, J.L., Farnum, N.R., and Doi, J.A. (2014). Applied Statistics for Engineers and Scientists, Cengage Learning. [3rd ed.]. CT 06902."},{"key":"ref_29","doi-asserted-by":"crossref","unstructured":"Das, S., and Ramanan, N. (2023). Region-specific heterogeneity in neuronal nuclear morphology in young, aged and in Alzheimer\u2019s disease mouse brains. Front. Cell Dev. Biol., 11.","DOI":"10.3389\/fcell.2023.1032504"},{"key":"ref_30","doi-asserted-by":"crossref","unstructured":"Caviedes, A., Varas-Godoy, M., Lafourcade, C., Sandoval, S., Bravo-Alegria, J., Kaehne, T., Massmann, A., Figueroa, J.P., Nualart, F., and Wyneken, U. (2017). Endothelial nitric oxide synthase is present in dendritic spines of neurons in primary cultures. Front. Cell. Neurosci., 11.","DOI":"10.3389\/fncel.2017.00180"},{"key":"ref_31","doi-asserted-by":"crossref","first-page":"188","DOI":"10.1186\/s12974-023-02870-2","article-title":"Microglial senescence contributes to female-biased neuroinflammation in the aging mouse hippocampus: Implications for Alzheimer\u2019s disease","volume":"20","author":"Pham","year":"2023","journal-title":"J. Neuroinflamm."},{"key":"ref_32","doi-asserted-by":"crossref","first-page":"154","DOI":"10.1111\/cns.12182","article-title":"Endothelial nitric oxide synthase protects neurons against ischemic injury through regulation of brain-derived neurotrophic factor expression","volume":"20","author":"Li","year":"2014","journal-title":"CNS Neurosci. Ther."},{"key":"ref_33","doi-asserted-by":"crossref","first-page":"960","DOI":"10.1097\/NEN.0b013e318232a379","article-title":"Stages of the pathologic process in Alzheimer disease: Age categories from 1 to 100 years","volume":"70","author":"Braak","year":"2011","journal-title":"J. Neuropathol. Exp. Neurol."},{"key":"ref_34","doi-asserted-by":"crossref","unstructured":"G\u00f6tz, J., Richter-Stretton, G., and Cruz, E. (2021). Therapeutic Ultrasound as a Treatment Modality for Physiological and Pathological Ageing Including Alzheimer\u2019s Disease. Pharmaceutics, 13.","DOI":"10.3390\/pharmaceutics13071002"},{"key":"ref_35","doi-asserted-by":"crossref","first-page":"1020","DOI":"10.1016\/j.neuron.2018.04.036","article-title":"Ultrasound Produces Extensive Brain Activation via a Cochlear Pathway","volume":"98","author":"Guo","year":"2018","journal-title":"Neuron"}],"container-title":["Brain Sciences"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.mdpi.com\/2076-3425\/16\/7\/757\/pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T11:23:00Z","timestamp":1784546580000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.mdpi.com\/2076-3425\/16\/7\/757"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,7,18]]},"references-count":35,"journal-issue":{"issue":"7","published-online":{"date-parts":[[2026,7]]}},"alternative-id":["brainsci16070757"],"URL":"https:\/\/doi.org\/10.3390\/brainsci16070757","relation":{},"ISSN":["2076-3425"],"issn-type":[{"value":"2076-3425","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,7,18]]}}}