Early role of vascular dysregulation on late-onset Alzheimer’s disease based on multifactorial data-driven analysis
Open accessAbstract
Multifactorial mechanisms underlying late-onset Alzheimer’s disease (LOAD) are poorly characterized from an integrative perspective. Here spatiotemporal alterations in brain amyloid-β deposition, metabolism, vascular, functional activity at rest, structural properties, cognitive integrity and peripheral proteins levels are characterized in relation to LOAD progression. We analyse over 7,700 brain images and tens of plasma and cerebrospinal fluid biomarkers from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Through a multifactorial data-driven analysis, we obtain dynamic LOAD–abnormality indices for all biomarkers, and a tentative temporal ordering of disease progression. Imaging results suggest that intra-brain vascular dysregulation is an early pathological event during disease development. Cognitive decline is noticeable from initial LOAD stages, suggesting early memory deficit associated with the primary disease factors. High abnormality levels are also observed for specific proteins associated with the vascular system’s integrity. Although still subjected to the sensitivity of the algorithms and biomarkers employed, our results might contribute to the development of preventive therapeutic interventions.
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Vascular alterations such as cerebrovascular resistance and hypoperfusion may precede amyloid deposition and are predictive of future disease progression.
“In support of this hypothesis, recent evidence from neuroimaging studies suggests that vascular alterations such as cerebrovascular resistance and hypoperfusion may precede amyloid deposition and are predictive of future disease progression (Iturria-Medina et al., 2016; Yew et al., 2017).”
From White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease (2018) · cites this paper as Iturria-Medina et al., 2016
The Discussion (page unavailable) says the modeled vascular abnormalities appear earlier than amyloid-β deposition, and the Methods describe cerebral blood-flow imaging. But the paper does not establish cerebrovascular resistance as an early marker or show that these alterations predict an individual’s future disease progression; its Discussion describes prediction as a potential use of the model. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAge-related vascular changes may influence disease progression in late-onset Alzheimer's disease, including the development of white matter alterations, which is less likely to be captured in autosomal dominant Alzheimer's disease where dementia symptoms typically emerge between 30 and 50 years of age.
“Age-related vascular changes may influence disease progression in late-onset Alzheimer’s disease, including the development of white matter alterations (Iturria-Medina et al., 2016), which is less likely to be captured in autosomal dominant Alzheimer’s disease where dementia symptoms typically emerge between 30 and 50 years of age.”
From White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease (2018) · cites this paper as Iturria-Medina et al., 2016
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredWMHs often occur prior to the presence of amyloid-β plaques in preclinical AD.
“findings from previous studies have also shown that WMHs often occur prior to the presence of amyloid-β plaques in preclinical AD [19,20,21]”
From Amyloid-PET and White Matter Hyperintensities Have Independent Effects on Baseline Cognitive Function and Synergistic Effects on Longitudinal Executive Function (2023) · cites this paper as [20]
The Results (Multifactorial biomarker ordering in LOAD progression) place vascular dysregulation before Aβ deposition. But the Discussion says the analysis did not evaluate white-matter alterations, so it does not establish that WMHs specifically precede amyloid plaques in preclinical AD or that this often occurs. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSome studies have suggested that during preclinical stages, vascular dysfunction is among the first detectable biomarker changes reported before symptomatic onset and before changes in other standard AD biomarkers, including amyloid deposition and CSF Aβ42, phosphorylated tau, and total tau.
“Some studies have suggested that during preclinical stages, vascular dysfunction is among the first detectable biomarker changes reported before symptomatic onset and before changes in other standard AD biomarkers, including amyloid deposition and CSF A 𝛃 42, phosphorylated tau (pTau), and total tau (285, 421).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [285]
The Results (‘Multifactorial biomarker ordering in LOAD progression’; page unavailable) place vascular dysregulation ahead of amyloid deposition in abnormality magnitude and compare it with CSF Aβ1–42, tau and ptau. But they report memory-impairment symptoms from very early disease stages; the paper does not establish that vascular changes were detected before symptomatic onset. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAD risk factors such as aging, hypertension, diabetes, and apolipoprotein E4 genotype lead to cerebrovascular damage, inducing blood-brain barrier damage and brain perfusion reduction.
“Hit one, the AD risk factors such as aging, hypertension, diabetes, and apolipoprotein E4 (ApoE4) genotype lead to cerebrovascular damage, inducing blood‐brain barrier (BBB) damage and brain perfusion reduction.[ 4 , 6 ]”
From Multifunctional Nanostructure RAP‐RL Rescues Alzheimer's Cognitive Deficits through Remodeling the Neurovascular Unit (2021) · cites this paper as [4]
The Discussion (page unavailable) reports age-dependent blood–brain barrier breakdown, and the Results discuss insulin-related and oxidative-stress pathways that may affect the barrier. The paper also studies cerebral blood flow as a measure of vascular dysregulation. It does not establish that hypertension, diabetes, and ApoE4 each cause cerebrovascular damage, nor that such damage causes both barrier damage and reduced perfusion; the Discussion explicitly cautions that its analysis does not reveal direct causal relationships. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Pathological investigations from 80% of patients diagnosed with AD but without evidence of mixed dementia exhibited pathogenic progression associated with various types of cerebrovascular dysfunction including lacunes, cortical infarcts, cerebral microbleeds, multiple microinfarcts, and intracranial atherosclerosis.
“Pathological investigations from 80% of patients diagnosed with AD but without evidence of mixed dementia exhibited pathogenic progression associated with various types of cerebrovascular dysfunction including lacunes, cortical infarcts, cerebral microbleeds, multiple microinfarcts, and intracranial atherosclerosis.[ 4 ]”
From Multifunctional Nanostructure RAP‐RL Rescues Alzheimer's Cognitive Deficits through Remodeling the Neurovascular Unit (2021) · cites this paper as [4]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredIn patients and mouse models of AD, fibrinogen extravasates in the brain at sites of impaired blood-brain barrier integrity and cerebrovascular dysfunction, which are early features of AD pathogenesis.
“In patients and mouse models of AD, fibrinogen extravasates in the brain at sites of impaired blood-brain barrier integrity and cerebrovascular dysfunction, which are early features of AD pathogenesis.21,39-42”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [39]
The Discussion (page not provided) says the paper’s results suggest vascular dysregulation is an early event in late-onset AD and notes evidence of blood–brain barrier permeability breakdown in the human hippocampus. It does not report fibrinogen extravasation at affected brain sites in patients or mouse models. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIt is possible that age-related cerebrovascular pathology may precede primary Alzheimer's disease pathology and contribute to white matter changes to a stronger degree in subjects with sporadic Alzheimer's disease compared to the relatively young subjects with autosomal-dominant Alzheimer's disease.
“It should be noted that although white matter changes were detected subsequent to amyloid and tau pathology in the current study, it is still possible that age-related cerebrovascular pathology may precede primary Alzheimer’s disease pathology (Iturria-Medina et al., 2016) and contribute to white matter changes to a stronger degree in subjects with sporadic Alzheimer’s disease compared to the”
From White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease (2018) · cites this paper as Iturria-Medina et al., 2016
Increasing evidence supports that early cerebrovascular dysfunction contributes to AD pathophysiology and cognitive impairment.
“In addition to the classic hallmark pathology, A 𝛃 plaques, hyperphosphorylated tau neurofibrillary tangles, and neuron loss, increasing evidence supports that early cerebrovascular dysfunction contributes to AD pathophysiology and cognitive impairment (29, 285, 418, 421, 429, 569, 571, 593, 682, 693).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [285]
Vascular pathology is part of the multifactorial mechanisms present in LOAD.
“Vascular pathology is also known to be part of the multifactorial mechanisms present in LOAD (Ortner et al., 2015; Iturria-Medina et al., 2016).”
From Effects of Alzheimer’s and Vascular Pathologies on Structural Connectivity in Early- and Late-Onset Alzheimer’s Disease (2021) · cites this paper as Iturria-Medina et al., 2016
Fibrinogen elevation in plasma and cerebrospinal fluid is an early biomarker of dementia risk and is associated with progression of cognitive decline in AD.
“Biomarker studies further support the notion that fibrinogen elevation in plasma and cerebrospinal fluid is an early biomarker of dementia risk and is associated with progression of cognitive decline in AD.39,45-48”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [39]
The Results section ('Peripheral vascular and inflammatory alterations'; page unavailable) discusses plasma and CSF proteins as potential early biomarkers, but identifies other analytes rather than fibrinogen. Searches for fibrinogen and for elevated plasma or CSF fibrinogen in relation to dementia risk or cognitive decline found no passage addressing the specific claim. (LLM, conf=0.75)
Experimental — accuracy not yet measuredCerebrovascular dysfunction is one of the earliest abnormalities detected in CAA, which also manifests in early stages of AD onset.
“Cerebrovascular dysfunction is one of the earliest abnormalities detected in CAA, which also manifests in early stages of AD onset [604].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [604]
Reduced cerebral blood flow is the earliest biomarker of the development of Alzheimer's disease.
“reduced cerebral blood flow is the earliest biomarker of the development of the disease (1).”
From Amyloid β oligomers constrict human capillaries in Alzheimer's disease via signaling to pericytes (2019) · cites this paper as [1]
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Ali, D. G., Abner, E. L., Bahrani, A. A., El Khouli, R., Gold, B. T., Jiang, Y., Wilcock, D. M., & Jicha, G. A. (2023) · Brain Sciences · doi:10.3390/brainsci13020218 · Cited by 7 · see citing works
- Authors
- Iturria-Medina, Y., Sotero, R. C., Toussaint, P. J., Mateos-Pérez, J. M., Evans, A. C., Initiative, T. A. D. N., Weiner, M. W., Aisen, P., Petersen, R., Jack, C. R., Jagust, W., Trojanowki, J. Q., Toga, A. W., Beckett, L., Green, R. C., Saykin, A. J., Morris, J., Shaw, L. M., Khachaturian, Z., Sorensen, G., Kuller, L., Raichle, M., Paul, S., Davies, P., Fillit, H., Hefti, F., Holtzman, D., Mesulam, M. M., Potter, W., Snyder, P., Schwartz, A., Montine, T., Thomas, R. G., Donohue, M., Walter, S., Gessert, D., Sather, T., Jiminez, G., Harvey, D., Bernstein, M., Fox, N., Thompson, P., Schuff, N., Borowski, B., Gunter, J., Senjem, M., Vemuri, P., Jones, D., Kantarci, K., Ward, C., Koeppe, R. A., Foster, N., Reiman, E. M., Chen, K., Mathis, C., Landau, S., Cairns, N. J., Householder, E., Taylor-Reinwald, L., Lee, V., Korecka, M., Figurski, M., Crawford, K., Neu, S., Foroud, T. M., Potkin, S., Shen, L., Faber, K., Kim, S., Nho, K., Thal, L., Buckholtz, N., Albert, M., Frank, R., Hsiao, J., Kaye, J., Quinn, J., Lind, B., Carter, R., Dolen, S., Schneider, L. S., Pawluczyk, S., Beccera, M., Teodoro, L., Spann, B. M., Brewer, J., Vanderswag, H., Fleisher, A., Heidebrink, J. L., Lord, J. L., Mason, S. S., Albers, C. S., Knopman, D., Johnson, K., Doody, R. S., Villanueva-Meyer, J., Chowdhury, M., Rountree, S., Dang, M., Stern, Y., Honig, L. S., Bell, K. L., Ances, B., Carroll, M., Leon, S., Mintun, M. A., Schneider, S., Oliver, A., Marson, D., Griffith, R., Clark, D., Geldmacher, D., Brockington, J., Roberson, E., Grossman, H., Mitsis, E., de Toledo-Morrell, L., Shah, R. C., Duara, R., Varon, D., Greig, M. T., Roberts, P., Albert, M., Onyike, C., D’Agostino, D., Kielb, S., Galvin, J. E., Cerbone, B., Michel, C. A., Rusinek, H., de Leon, M. J., Glodzik, L., De Santi, S., Doraiswamy, P. M., Petrella, J. R., Wong, T. Z., Arnold, S. E., Karlawish, J. H., Wolk, D., Smith, C. D., Jicha, G., Hardy, P., Sinha, P., Oates, E., Conrad, G., Lopez, O. L., Oakley, M., Simpson, D. M., Porsteinsson, A. P., Goldstein, B. S., Martin, K., Makino, K. M., Ismail, M. S., Brand, C., Mulnard, R. A., Thai, G., Mc-Adams-Ortiz, C., Womack, K., Mathews, D., Quiceno, M., Diaz-Arrastia, R., King, R., Weiner, M., Martin-Cook, K., DeVous, M., Levey, A. I., Lah, J. J., Cellar, J. S., Burns, J. M., Anderson, H. S., Swerdlow, R. H., Apostolova, L., Tingus, K., Woo, E., Silverman, D. H. S., Lu, P. H., Bartzokis, G., Graff-Radford, N. R., Parfitt, F., Kendall, T., Johnson, H., Farlow, M. R., Hake, A., Matthews, B. R., Herring, S., Hunt, C., van Dyck, C. H., Carson, R. E., MacAvoy, M. G., Chertkow, H., Bergman, H., Hosein, C., Black, S., Stefanovic, B., Caldwell, C., Hsiung, G.-Y. R., Feldman, H., Mudge, B., Assaly, M., Kertesz, A., Rogers, J., Bernick, C., Munic, D., Kerwin, D., Mesulam, M.-M., Lipowski, K., Wu, C.-K., Johnson, N., Sadowsky, C., Martinez, W., Villena, T., Turner, R. S., Johnson, K., Reynolds, B., Sperling, R. A., Johnson, K. A., Marshall, G., Frey, M., Lane, B., Rosen, A., Tinklenberg, J., Sabbagh, M. N., Belden, C. M., Jacobson, S. A., Sirrel, S. A., Kowall, N., Killiany, R., Budson, A. E., Norbash, A., Johnson, P. L., Allard, J., Lerner, A., Ogrocki, P., Hudson, L., Fletcher, E., Carmichael, O., Olichney, J., DeCarli, C., Kittur, S., Borrie, M., Lee, T.-Y., Bartha, R., Johnson, S., Asthana, S., Carlsson, C. M., Potkin, S. G., Preda, A., Nguyen, D., Tariot, P., Reeder, S., Bates, V., Capote, H., Rainka, M., Scharre, D. W., Kataki, M., Adeli, A., Zimmerman, E. A., Celmins, D., Brown, A. D., Pearlson, G. D., Blank, K., Anderson, K., Santulli, R. B., Kitzmiller, T. J., Schwartz, E. S., Sink, K. M., Williamson, J. D., Garg, P., Watkins, F., Ott, B. R., Querfurth, H., Tremont, G., Salloway, S., Malloy, P., Correia, S., Rosen, H. J., Miller, B. L., Mintzer, J., Spicer, K., Bachman, D., Finger, E., Pasternak, S., Rachinsky, I., Drost, D., Pomara, N., Hernando, R., Sarrael, A., Schultz, S. K., Ponto, L. L. B., Shim, H., Smith, K. E., Relkin, N., Chaing, G., Raudin, L., Smith, A., Fargher, K., Raj, B. A., Neylan, T., Grafman, J., Davis, M., Morrison, R., Hayes, J., Finley, S., Friedl, K., Fleischman, D., Arfanakis, K., James, O., Massoglia, D., Fruehling, J. J., Harding, S., Peskind, E. R., Petrie, E. C., Li, G., Yesavage, J. A., Taylor, J. L., & Furst, A. J.
- Affiliations
- University of Calgary (CA)
- Montreal Neurological Institute and Hospital (CA)
- University of California, San Francisco (US)
- Mayo Clinic (US)
- University of Pennsylvania (US)
- University of Southern California (US)
- Brigham and Women's Hospital (US)
- Washington University in St. Louis (US)
- University of California San Diego (US)
- Siemens (Germany) (DE)
- University of Pittsburgh (US)
- Albert Einstein College of Medicine (US)
- Alzheimer's Drug Discovery Foundation (US)
- Northwestern University (US)
- Brown University (US)
- Eli Lilly (United States) (US)
- University of Washington (US)
- University of London (GB)
- University of California, Los Angeles (US)
- University of Utah (US)
- Banner Alzheimer’s Institute (US)
- University of Michigan (US)
- Indiana University Bloomington (US)
- National Institutes of Health (US)
- Johns Hopkins University (US)
- Oregon Health & Science University (US)
- Baylor College of Medicine (US)
- University of Alabama at Birmingham (US)
- Icahn School of Medicine at Mount Sinai (US)
- Rush University Medical Center (US)
- New York University (US)
- Duke Medical Center (US)
- University of Kentucky (US)
- University of Rochester Medicine (US)
- University of California, Irvine (US)
- The University of Texas Southwestern Medical Center (US)
- Emory University (US)
- University of Kansas Medical Center (US)
- Yale University (US)
- Jewish General Hospital (CA)
- Sunnybrook Health Science Centre (CA)
- Cleveland Clinic (US)
- St Joseph's Health Care (CA)
- Palm Beach Neurology (US)
- Georgetown University Medical Center (US)
- Banner Sun Health Research Institute (US)
- Boston University (US)
- Howard University (US)
- Case Western Reserve University (US)
- University of California, Davis (US)
- University of Wisconsin–Madison (US)
- Dent Neurologic Institute (US)
- The Ohio State University (US)
- Albany Medical College (US)
- Hartford Hospital (US)
- Dartmouth–Hitchcock Medical Center (US)
- Wake Forest University Health Sciences (US)
- Rhode Island Hospital (US)
- Butler Hospital (US)
- Medical University of South Carolina (US)
- Nathan Kline Institute for Psychiatric Research (US)
- University of Iowa (US)
- Cornell University (US)
- University of South Florida (US)
- Stanford University (US)
- Corresponding author
- Evans, A. C.
- ORCID
- Sotero, R. C.
- Toussaint, P. J.
- Mateos-Pérez, J. M.
- Evans, A. C.
- Weiner, Michael W.
- Petersen, Ronald
- Jack, Clifford R.
- Jagust, William
- Toga, Arthur W.
- Beckett, Laurel
- Green, Robert C.
- Saykin, Andrew J.
- Morris, John
- Shaw, Leslie M.
- Paul, Steven
- Davies, Peter
- Fillit, Howard
- Hefti, Franz
- Snyder, Peter
- Thomas, Ronald G.
- Donohue, Michael
- Walter, Sarah
- Harvey, Danielle
- Fox, Nick
- Thompson, Paul
- Vemuri, Prashanthi
- Jones, David
- Kantarci, Kejal
- Koeppe, Robert A.
- Reiman, Eric M.
- Chen, Kewei
- Korecka, Magdalena
- Crawford, Karen
- Foroud, Tatiana M.
- Shen, Li
- Faber, Kelley
- Kim, Sungeun
- Nho, Kwangsik
- Frank, Richard
- Hsiao, John
- Kaye, Jeffrey
- Quinn, Joseph
- Schneider, Lon S.
- Fleisher, Adam
- Heidebrink, Judith L.
- Lord, Joanne L.
- Knopman, David
- Johnson, Kris
- Stern, Yaakov
- Honig, Lawrence S.
- Bell, Karen L.
- Ances, Beau
- Carroll, Maria
- Oliver, Angela
- Marson, Daniel
- Clark, David
- Geldmacher, David
- Roberson, Erik
- Shah, Raj C.
- Duara, Ranjan
- Albert, Marilyn
- Onyike, Chiadi
- D’Agostino, Daniel
- Kielb, Stephanie
- Galvin, James E.
- Cerbone, Brittany
- Rusinek, Henry
- Glodzik, Lidia
- Doraiswamy, P. Murali
- Petrella, Jeffrey R.
- Wong, Terence Z.
- Arnold, Steven E.
- Karlawish, Jason H.
- Wolk, David
- Smith, Charles D.
- Hardy, Peter
- Sinha, Partha
- Porsteinsson, Anton P.
- Ismail, M. Saleem
- Thai, Gaby
- Womack, Kyle
- Quiceno, Mary
- Diaz-Arrastia, Ramon
- Weiner, Myron
- DeVous, Michael
- Levey, Allan I.
- Lah, James J.
- Burns, Jeffrey M.
- Swerdlow, Russell H.
- Apostolova, Liana
- Silverman, Daniel H. S.
- Lu, Po H.
- Johnson, Heather
- Farlow, Martin R.
- Carson, Richard E.
- Chertkow, Howard
- Bergman, Howard
- Black, Sandra
- Stefanovic, Bojana
- Hsiung, Ging-Yuek Robin
- Feldman, Howard
- Bernick, Charles
- Kerwin, Diana
- Johnson, Nancy
- Turner, Raymond Scott
- Sperling, Reisa A.
- Johnson, Keith A.
- Marshall, Gad
- Frey, Meghan
- Lane, Barton
- Rosen, Allyson
- Sabbagh, Marwan N.
- Belden, Christine M.
- Jacobson, Sandra A.
- Kowall, Neil
- Killiany, Ronald
- Budson, Andrew E.
- Norbash, Alexander
- Lerner, Alan
- Fletcher, Evan
- Carmichael, Owen
- Olichney, John
- DeCarli, Charles
- Johnson, Sterling
- Asthana, Sanjay
- Carlsson, Cynthia M.
- Preda, Adrian
- Nguyen, Dana
- Tariot, Pierre
- Scharre, Douglas W.
- Kataki, Maria
- Pearlson, Godfrey D.
- Santulli, Robert B.
- Sink, Kaycee M.
- Williamson, Jeff D.
- Garg, Pradeep
- Ott, Brian R.
- Tremont, Geoffrey
- Salloway, Stephen
- Correia, Stephen
- Miller, Bruce L.
- Mintzer, Jacobo
- Bachman, David
- Pasternak, Stephen
- Pomara, Nunzio
- Schultz, Susan K.
- Ponto, Laura L. Boles
- Shim, Hyungsub
- Relkin, Norman
- Smith, Amanda
- Neylan, Thomas
- Grafman, Jordan
- Hayes, Jacqueline
- Friedl, Karl
- Fleischman, Debra
- Arfanakis, Konstantinos
- Peskind, Elaine R.
- Petrie, Eric C.
- Yesavage, Jerome A.
- Taylor, Joy L.
- Furst, Ansgar J.
- Venue
- Nature Communications
- Published
- 2016-06-21
- Volume
- 7
- Issue
- 1
- Pages
- 11934-11934
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4919512
- OpenAlex
- W2474981734
- Cited by
- 1,202
- References
- 63
- Citations by year
- 2026: 127 · 2025: 139 · 2024: 108 · 2023: 129 · 2022: 136 · 2021: 153 · 2020: 142 · 2019: 110 · 2018: 81 · 2017: 65 · 2016: 11
- FWCI
- 79.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Scholarship@Western (Western University) (submittedVersion)
- Columbia Academic Commons (Columbia University)
- Funders
- U.S. Department of Defense (U01 AG024904, W81XWH, W81XWH-12-2-, W81XWH-12, W81XWH1220012, AG024904)
- Foundation for the National Institutes of Health (W81XWH-12-2-0012, U01AG024904, Grant U01 AG024904, AG024904)
- Alzheimer's Association (U01 AG024904, W81XWH-12-2-0012)
- Bristol-Myers Squibb (U01 AG024904, AG024904, W81XWH-12-2-0012)
- Eli Lilly and Company (U01 AG024904, AG024904, W81XWH-12-2-0012)
- Pfizer (AG024904, W81XWH-12-2-0012, U01 AG024904)
- Biogen (W81XWH-12-2-0012, U01 AG024904, AG024904)
- University of Southern California (W81XWH-12-2-0012, U01 AG024904)
- F. Hoffmann-La Roche (W81XWH-12-2-0012, AG024904, U01 AG024904)
- Meso Scale Diagnostics (U01 AG024904, AG024904, W81XWH-12-2-0012)
- Alzheimer's Disease Neuroimaging Initiative (W81XWH-12-2–0012, U01AG024904, AG024904, W81XWH-12-2-, Department of Defense award number W81XWH-12-2-0012)
- BioClinica (U01 AG024904, W81XWH-12-2-0012, AG024904)
- Novartis Pharmaceuticals Corporation (W81XWH-12-2-0012, U01 AG024904, AG024904)
- Fondation Brain Canada
- Northern California Institute for Research and Education (U01 AG024904, W81XWH-12-2-0012)
- Eisai (W81XWH-12-2-0012, U01 AG024904, AG024904)
- Azrieli Foundation (BC_Azrieli_MIRI_3388)
- Servier (AG024904, W81XWH-12-2-0012, U01 AG024904)
- H. Lundbeck A/S (U01 AG024904, AG024904, W81XWH-12-2-0012)
- IXICO (AG024904, W81XWH-12-2-0012, U01 AG024904)
- National Institutes of Health (3u01ag024904-10s2, W81XWH, W81XWH-12-2-0012, U01-AG024904, Grant U01 AG024904, AG024904)
- Genentech (W81XWH-12-2-0012, AG024904, U01 AG024904)
- University of California, San Diego
- Canadian Institutes of Health Research (U01 AG024904, W81XWH-12-2-0012)
- National Institute on Aging (U01-AG-024904, W81XWH-12-2–0012, AG 024904, P50AG005142, P50AG005136, U24AG021886)
- National Institute of Biomedical Imaging and Bioengineering (W81XWH-12-2-0012, U01 AG024904, AG024904)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- late-onset Alzheimer's disease, vascular dysregulation, amyloid-beta deposition, brain metabolism, resting-state functional connectivity, cognitive decline, memory impairment, cerebrospinal fluid biomarkers, plasma biomarkers, disease progression, ADNI
- MeSH terms
- Aged, Alzheimer Disease, Blood Proteins, Brain, Brain Mapping, Cerebrovascular Circulation, Female, Glucose, Humans, Image Interpretation, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Models, Statistical, Biomarkers, Multivariate Analysis, Amyloid beta-Peptides, tau Proteins, Disease Progression, Positron-Emission Tomography, Neuroimaging, Cognitive Dysfunction
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