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Despite accumulating evidence on the clinical prognostic value of tau PET in typical late-onset amnestic AD, its utility in predicting clinical decline in individuals with atypical forms of AD remains unclear. Across heterogeneous clinical phenotypes, patients with atypical AD consistently exhibit abnormal tau accumulation in the posterior nodes of the default mode network of the cerebral cortex. This evidence suggests that tau burden in this functional network could be a common imaging biomarker for prognostication across the syndromic spectrum of AD.<\/jats:p>\n                  <jats:p>Here, we examined the relationship between baseline tau PET signal and the rate of subsequent clinical decline in a sample of 48 A+\/T+\/N+ patients with mild cognitive impairment or mild dementia due to AD with atypical clinical phenotypes: Posterior Cortical Atrophy (n = 16); logopenic variant Primary Progressive Aphasia (n = 15); and amnestic syndrome with multi-domain impairment and young age of onset &amp;lt; 65 years (n = 17). All patients underwent MRI, tau PET and amyloid PET scans at baseline. Each patient\u2019s longitudinal clinical decline was assessed by calculating the annualized change in the Clinical Dementia Rating Sum-of-Boxes (CDR-SB) scores from baseline to follow-up (mean time interval = 14.55 \u00b1 3.97 months).<\/jats:p>\n                  <jats:p>Atypical early AD patients showed an increase in CDR-SB by 1.18 \u00b1 1.25 points per year: t(47) = 6.56, P &amp;lt; 0.001, Cohen\u2019s d = 0.95. Across clinical phenotypes, baseline tau in the default mode network was the strongest predictor of clinical decline (R2 = 0.30), outperforming a simpler model with baseline clinical impairment and demographic variables (R2 = 0.10), tau in other functional networks (R2 = 0.11\u20130.26) and the magnitude of cortical atrophy (R2 = 0.20) and amyloid burden (R2 = 0.09) in the default mode network.<\/jats:p>\n                  <jats:p>Overall, these findings point to the contribution of default mode network tau to predicting the magnitude of clinical decline in atypical early AD patients 1 year later. This simple measure could aid the development of a personalized prognostic, monitoring and treatment plan, which would help clinicians not only predict the natural evolution of the disease but also estimate the effect of disease-modifying therapies on slowing subsequent clinical decline given the patient\u2019s tau burden while still early in the disease course.<\/jats:p>","DOI":"10.1093\/brain\/awae327","type":"journal-article","created":{"date-parts":[[2024,10,14]],"date-time":"2024-10-14T23:19:54Z","timestamp":1728947994000},"page":"1329-1344","source":"Crossref","is-referenced-by-count":27,"title":["Default mode network tau predicts future clinical decline in atypical early Alzheimer\u2019s disease"],"prefix":"10.1093","volume":"148","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0413-747X","authenticated-orcid":false,"given":"Yuta","family":"Katsumi","sequence":"first","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]},{"name":"Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital , Charlestown, MA 02129 ,","place":["USA"]},{"name":"Alzheimer\u2019s Disease Research Center, Massachusetts General Hospital , Charlestown, MA 02129 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Inola A","family":"Howe","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan","family":"Eckbo","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bonnie","family":"Wong","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]},{"name":"Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megan","family":"Quimby","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daisy","family":"Hochberg","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott M","family":"McGinnis","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]},{"name":"Center for Brain\/Mind Medicine, Department of Neurology, Brigham & Women\u2019s Hospital , Boston, MA 02115 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5575-5572","authenticated-orcid":false,"given":"Deepti","family":"Putcha","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]},{"name":"Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]},{"name":"Center for Brain\/Mind Medicine, Department of Neurology, Brigham & Women\u2019s Hospital , Boston, MA 02115 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A","family":"Wolk","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Pennsylvania , Philadelphia, PA 19104 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandra","family":"Touroutoglou","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]},{"name":"Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital , Charlestown, MA 02129 ,","place":["USA"]},{"name":"Alzheimer\u2019s Disease Research Center, Massachusetts General Hospital , Charlestown, MA 02129 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5958-3445","authenticated-orcid":false,"given":"Bradford C","family":"Dickerson","sequence":"additional","affiliation":[{"name":"Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]},{"name":"Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital , Charlestown, MA 02129 ,","place":["USA"]},{"name":"Alzheimer\u2019s Disease Research Center, Massachusetts General Hospital , Charlestown, MA 02129 ,","place":["USA"]},{"name":"Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School , Boston, MA 02114 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,10,16]]},"reference":[{"key":"2025040316581664900_awae327-B1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/j.jalz.2011.10.007","article-title":"National Institute on Aging\u2013Alzheimer\u2019s Association guidelines for the neuropathologic assessment of Alzheimer\u2019s disease","volume":"8","author":"Hyman","year":"2012","journal-title":"Alzheimers 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