Citations 4
Relationships of CSF biomarkers to cortical atrophy in early‐onset Alzheimer's disease
Touroutoglou, Alexandra, Katsumi, Yuta, Hensel, Jennifer, Schindler, Suzanne E., Ibanez, Laura, Brickhouse, Michael, Eloyan, Ani, Eckbo, Ryan, Zaitsev, Alexander, Joie, Renaud La, Thangarajah, Maryanne, Taurone, Alexander, Vemuri, Prashanthi, Jack, Clifford R., Hammers, Dustin B., Foroud, Tatiana, Aisen, P, Ls, Beckett, Koeppe, Robert, Kukull, Walter A., Toga, Arthur, ATRI, A, Db, Clark, Day, Gregory S., Duara, Ranjan, Graff‐Radford, Neill R., Grant, Ian M., Ls, Honig, Johnson, Erik C. B., Jones, David T., Masdeu, J C, Mf, Mendez, Musiek, Erik, Onyike, Chiadi U., Riddle, Meghan, Rogalski, Emily, Salloway, Stephen, Sha, Sharon, Turner, R. Scott, Wingo, Thomas S., D, Von Dem Wolk, Womack, Kyle, Carrillo, Maria C., Rabinovici, Gil D., Apostolova, L G, JL, Dage, Dickerson, Bradford C., Eldaief, Mark C., Joie, Renaud La , La Joie, Renaud , Touroutoglou, Alexandra , Katsumi, Yuta , Schindler, Suzanne E. , Ibanez, Laura , Brickhouse, Michael , Eloyan, Ani , Thangarajah, Maryanne, Vemuri, Prashanthi , Jack, Clifford R. , Hammers, Dustin B , Foroud, Tatiana , Aisen, Paul , Beckett, Laurel, Koeppe, Robert A. , Kukull, Walter A. , Toga, Arthur W. , Atri, Alireza, Clark, David, Day, Gregory S. , Duara, Ranjan , Graff‐Radford, Neill R. , Johnson, Erik C. B. , Jones, David T. , Musiek, Erik , Onyike, Chiadi U. , Riddle, Meghan , Salloway, Stephen , Sha, Sharon J. , Turner, R. Scott, Wingo, Thomas S , Wolk, David A. , Womack, Kyle , Carrillo, María C. , Rabinovici, Gil D. , Apostolova, Liana G. , Dickerson, Bradford Clark , Eldaief, Mark C.
Alzheimer's & Dementia | July 21, 2026 | Volume: 22 | Issue: 7 | Pages: No page available
Abstract INTRODUCTION Although cerebrospinal fluid (CSF) biomarkers reflect neurodegeneration in Alzheimer's disease (AD), it remains unclear whether these biomarkers track neurodegeneration in early‐onset Alzheimer's disease (EOAD). METHODS In 80 EOAD patients, we examined correlations between eight CSF biomarker levels and cortical thickness decreases within the EOAD cortical atrophy signature. Significant correlations were then entered into a multiple regression analysis. We also examined contributions of EOAD atrophy and CSF biomarkers to cognitive impairment. RESULTS The levels of four CSF biomarkers correlated to EOAD signature atrophy. Stepwise regression analyses revealed that CSF neurofilament light chain (NfL) levels best predicted EOAD signature atrophy. Multiple regression showed EOAD signature atrophy combined with CSF NfL levels explained more variance in cognitive impairment than either factor alone. DISCUSSION Within EOAD patients, CSF NfL levels relate to the magnitude of cortical atrophy, and a combination of EOAD signature atrophy and CSF NfL levels most robustly predict cognitive impairment.
Cognitive dispersion profiles and prediction of cognitive change in early‐onset dementias: Results from LEADS
Hammers, Dustin B., Foster, Elodie, Eloyan, Ani, Thangarajah, Maryanne, Taurone, Alexander, Touroutoglou, Alexandra, Joie, Renaud La, Beckett, Laurel, Gao, Sujuan, Vemuri, Prashanthi, Nudelman, Kelly N., Kirby, Kala, Dage, Jeffrey L., Aisen, Paul, Atri, Alireza, Clark, David G., Day, Gregory S., Duara, Ranjan, Graff‐Radford, Neill R., Grant, Ian, Honig, Lawrence S., Johnson, Erik C. B., Jones, David T., Masdeu, Joseph C., Mendez, Mario F., Parand, Leila, Womack, Kyle, Musiek, Erik, Onyike, Chiadi U., Riddle, Meghan, Rogalski, Emily, Salloway, Stephen, Sha, Sharon J., Turner, Raymond Scott, Wingo, Thomas S., Wolk, David A., Dickerson, Bradford C., Rabinovici, Gil D., Carrillo, Maria C., Apostolova, Liana G., Joie, Renaud La , La Joie, Renaud , Hammers, Dustin B , Eloyan, Ani , Thangarajah, Maryanne, Taurone, Alexander, Touroutoglou, Alexandra , Beckett, Laurel , Gao, Sujuan , Vemuri, Prashanthi , Nudelman, Kelly , Kirby, Kala, Dage, Jeffrey L. , Aisen, Paul , Atri, Alireza , Day, Gregory S. , Duara, Ranjan , Graff‐Radford, Neill R. , Honig, Lawrence S. , Johnson, Erik C. B. , Jones, David T. , Masdeu, Joseph C , Mendez, Mario F. , Womack, Kyle , Musiek, Erik , Onyike, Chiadi U. , Riddle, Meghan , Rogalskı, Emily , Salloway, Stephen, Sha, Sharon J. , Turner, Raymond Scott , Wingo, Thomas S , Wolk, David A. , Dickerson, Bradford Clark , Rabinovici, Gil D. , Carrillo, María C. , Apostolova, Liana G.
Alzheimer's & Dementia | May 19, 2026 | Volume: 22 | Issue: 5 | Pages: No page available
Abstract INTRODUCTION Research into cognitive dispersion – a cognitive process score measuring the intra‐individual variability (IIV) across a single testing session – suggests utility in neurodegenerative populations. Given widespread deficits observed in sporadic early‐onset Alzheimer's disease (EOAD), however, it is unclear if examining cognitive dispersion shows benefit in this condition. METHODS A total of 309 participants (188 amyloid‐positive EOAD, 43 amyloid‐negative early‐onset dementia [EOnonAD], 78 cognitively normal [CN]) completed neuropsychological testing twice over 12 months. Dispersion‐related differences among groups were assessed, as was cognitive dispersion's capacity to predict domain‐specific cognitive trajectories, and its convergence with imaging biomarkers. RESULTS EOAD participants displayed higher cognitive dispersion than EOnonAD participants, and associations with EOAD‐specific biomarkers. Additionally, cognitive dispersion was associated with 12‐month reliable change across several cognitive domains. DISCUSSION These preliminary results examine cognitive dispersion in sporadic EOAD. When used with baseline cognitive performance, cognitive dispersion measures may enrich future clinical trials in EOAD by enhancing treatment monitoring over time.
Criterion and convergent validity of plasma biomarkers in early‐onset Alzheimer's disease: Initial findings from LEADS
Hammers, Dustin B., Polsinelli, Angelina, Eloyan, Ani, Taurone, Alexander, Thangarajah, Maryanne, Foroud, Tatiana, Gao, Sujuan, Beckett, Laurel, Joie, Renaud La, Touroutoglou, Alexandra, Vemuri, Prashanthi, Zetterberg, Henrik, Blennow, Kaj, Nemes, Sára , Костадинова, Ралица, Aisen, Paul, Nudelman, Kelly N., Kirby, Kala, Atri, Alireza, Clark, David, Day, Gregory S., Duara, Ranjan, Graff‐Radford, Neill R., Grant, Ian, Honig, Lawrence S., Johnson, Erik C. B., Jones, David T., Masdeu, Joseph C., Mendez, Mario F., Parand, Leila, Womack, Kyle, Musiek, Erik, Onyike, Chiadi U., Riddle, Meghan, Rogalskı, Emily , Salloway, Stephen, Sha, Sharon J., Turner, Raymond Scott, Wingo, Thomas S., Wolk, David A., Carrillo, Maria C., Rabinovici, Gil D., Dickerson, Bradford C., Dage, Jeffrey L., Apostolova, Liana G., Carrillo, María C. , Rabinovici, Gil D. , Joie, Renaud La , Polsinelli, Angelina J. , La Joie, Renaud , Rabinovici, Gil D , Hammers, Dustin B , Eloyan, Ani , Taurone, Alexander, Thangarajah, Maryanne, Foroud, Tatiana , Gao, Sujuan , Beckett, Laurel , Touroutoglou, Alexandra , Vemuri, Prashanthi , Zetterberg, Henrik , Blennow, Kaj , Kostadinova, Ralitsa, Aisen, Paul , Nudelman, Kelly , Kirby, Kala, Atri, Alireza , Clark, David, Day, Gregory S. , Duara, Ranjan , Graff‐Radford, Neill R. , Honig, Lawrence S. , Johnson, Erik C. B. , Jones, David T. , Masdeu, Joseph C , Mendez, Mario F. , Womack, Kyle , Musiek, Erik , Onyike, Chiadi U. , Riddle, Meghan , Salloway, Stephen , Sha, Sharon J. , Turner, Raymond Scott , Wingo, Thomas S , Wolk, David A. , Dickerson, Bradford Clark , Dage, Jeffrey L. , Apostolova, Liana G.
Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring | May 4, 2026 | Volume: 18 | Issue: 2 | Pages: No page available
Abstract INTRODUCTION : Despite expanding use of plasma biomarkers for Alzheimer's disease (AD), minimal examination has been undertaken in early‐onset AD (EOAD). Prior analyses assessed criterion and convergent validity of common plasma biomarkers in a well‐characterized sample with sporadic EOAD. METHODS : Plasma amyloid beta (Aβ) 42/40, tau phosphorylated at threonine 231 (p‐tau231), glial fibrillary acidic protein (GFAP), and neurofilament light change (NfL) levels were obtained for 189 EOAD, 52 early‐onset non‐AD (EOnonAD), and 83 cognitively normal (CN) participants. Diagnostic group differences, convergence with imaging biomarkers, and the capacity to predict specific cognitive domains were investigated. RESULTS : After controlling for cognitive status, EOAD participants exhibited more pathologic levels of Aβ42/40, p‐tau231, and GFAP relative to EOnonAD participants. However, NfL displayed the greatest sensitivity to non‐amnestic cognitive impairment across the sample. DISCUSSION : These results establish criterion and convergent validity of plasma biomarkers in sporadic EOAD and highlight complementary roles that AD‐specific and non‐specific plasma markers may play across the course of AD care.
Distinct Tau PET Dynamics in Early vs. Late Age-of-Onset Alzheimer’s disease
Chiotis, Konstantinos, Soleimani-Meigooni, David N, Aisen, Paul S, Amuiri, Alinda, Atri, Alireza, Beckett, Laurel, Brickhouse, Michael , Clark, David G, Dage, Jeffrey L, Day, Gregory S, Duara, Ranjan, Eloyan, Ani , Foroud, Tatiana, Graff-Radford, Neill R, Grant, Ian M, Hammers, Dustin B, Honig, Lawrence S, Johnson, Erik C. B., Jones, D. Richard, Kirby, Kala, Koeppe, Robert, Kramer, Joel H, Kukull, Walter A, Leuzy, Antoine , Masdeu, Joseph C., Mendez, Mario F., Musiek, Erik, Nudelman, Kelly N., Onyike, Chiadi U., Riddle, Meghan, Rocha, Salma, Rogalski, Emily, Salloway, Stephen, Schonhaut, Daniel R., Sha, Sharon, Shankar, Ranjani, Taurone, Alexander, Thangarajah, Maryanne, Toga, Arthur W., Touroutoglou, Alexandra, Turner, Raymond Scott, Vemuri, Prashanthi, Wingo, Thomas S., Wolk, David A., Womack, Kyle, Zhang, J. , Carrillo, Maria C., Dickerson, Bradford C., Apostolova, Liana G., Joie, Renaud La, Rabinovici, Gil D., Chiotis, Konstantinos , Blazhenets, Ganna , Soleimani‐Meigooni, David N. , Aisen, Paul , Atri, Alireza , Beckett, Laurel , Clark, David G., Dage, Jeffrey L. , Day, Gregory S. , Duara, Ranjan , Foroud, Tatiana , Graff‐Radford, Neill R. , Hammers, Dustin B , Honig, Lawrence S. , Johnson, Erik C. B. , Jones, David T. , Koeppe, Robert A. , Kramer, Joel H. , Kukull, Walter A. , Lagarde, Julien , Maiti, Piyush , Masdeu, Joseph C , Mendez, Mario F. , Musiek, Erik , Nudelman, Kelly , Onyike, Chiadi U. , Riddle, Meghan , Rogalskı, Emily , Salloway, Stephen, Schonhaut, Daniel R. , Sha, Sharon J. , Shankar, Ranjani , Taurone, Alexander, Thangarajah, Maryanne, Toga, Arthur W. , Touroutoglou, Alexandra , Turner, Raymond Scott , Vemuri, Prashanthi , Wingo, Thomas S , Wolk, David A. , Womack, Kyle , Carrillo, María C. , Dickerson, Bradford Clark , Apostolova, Liana G. , Joie, Renaud La , Rabinovici, Gil D.
No container title available | January 26, 2026 | Volume: No volume available | Issue: No issue available | Pages: No page available
Abstract Early-onset Alzheimer’s disease (EOAD) and Late-onset AD (LOAD) differ in clinical presentations and rates of progression. We aimed to compare baseline and longitudinal tau PET burden, and their relationship with clinical variables in amyloid-PET positive, cognitively impaired participants from the Longitudinal Early-Onset Alzheimer’s Disease Study (EOAD; n=390) and Alzheimer’s Disease Neuroimaging Initiative (LOAD; n=211). Patients with EOAD showed higher baseline tau PET retention, broader neuroanatomical involvement and faster accumulation rates over time compared to LOAD, after adjusting for amyloid load and clinical stage. Tau PET showed stronger correlations with baseline amyloid burden and clinical measures of global cognition and function in EOAD than LOAD. We conclude that earlier age of onset in AD is linked to a more aggressive tauopathy, which in turn is a primary driver of clinical decline. These findings suggest that optimal therapeutic targets and strategies may differ between EOAD and LOAD. One Sentence Summary Younger patients with Alzheimer’s disease show more aggressive tau spread, suggesting age of onset defines distinct disease pathways with key clinical implications.