Cited by 5Alzheimer's disease research and treatmentsIntracerebral and Subarachnoid Hemorrhage ResearchNeurological Disease Mechanisms and Treatments

Tau depletion diminishes vascular amyloid-related deficits in a mouse model of cerebral amyloid angiopathy

Open access
Jury‐Garfe, Nur, Chimal‐Juárez, Enrique, Patel, Henika, Martinez‐Pinto, Jonathan, Vanderbosch, Kathryn, Mardones, Muriel D., Perkins, Abigail, Prisco, Gonzalo Viana Di +4 more·2025·Alzheimer's & Dementia

Abstract

INTRODUCTION: Tau is essential for amyloid beta (Aβ)–induced synaptic and cognitive deficits in Alzheimer's disease (AD), making its downregulation a therapeutic target. Cerebral amyloid angiopathy (CAA), a major vascular contributor to cognitive decline, affects over 90% of patients with AD. This study explores the impact of tau downregulation on CAA pathogenesis. METHODS: We crossed the Familial Danish Dementia mouse model (Tg‐FDD), which develops vascular amyloid, with tau‐null (mTau −/− ) mice to generate a CAA model lacking endogenous tau (Tg‐FDD/mTau −/− ). Behavioral, electrophysiological, histological, and transcriptomic analyses were performed. RESULTS: Tau depletion ameliorated motor and synaptic impairments, reduced vascular amyloid deposition, and prevented vascular damage. Tau ablation also mitigated astrocytic reactivity and neuroinflammation associated with vascular amyloid accumulation. CONCLUSION: These findings provide the first in vivo evidence of the beneficial effects of tau downregulation in a CAA mouse model, supporting tau reduction as a potential therapeutic strategy for patients with parenchymal and vascular amyloid deposition. Highlights: Tau ablation improves motor function and synaptic impair, reduces cerebrovascular amyloid deposits, and prevents vascular damage in a mouse model of cerebral amyloid angiopathy (CAA). Tau reduction decreases astrocytic reactivity, alters neuroinflammatory gene expression, and enhances oligodendrocyte function, suggesting a protective role against neuroinflammation in CAA. These findings highlight tau reduction as a potential therapeutic strategy to mitigate CAA‐induced pathogenesis, with implications for treating patients with both parenchymal and vascular amyloid deposition.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1002/alz.70238

Cites

9 of 9 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Tg-FDD mice present motor impairment, vascular damage, astrocytic reactivity and altered inflammation pathways in a sex dependent manner, with males exhibiting stronger phenotype.

    “Mice present motor impairment, vascular damage, astrocytic reactivity and altered inflammation pathways in a sex dependent manner, with males exhibiting stronger phenotype [85].”

    From Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease (2026) · cites this paper as [85]

    The Results sections on motor strength, vascular damage, and astrocytic reactivity report reduced grip strength in Tg-FDD mice, while vascular damage and astrocytic reactivity were observed only in males. The inflammation Results report altered inflammatory genes and pathways, but that analysis included only males; the reported motor-strength findings also do not establish a stronger male phenotype. Thus, the source does not support applying the sex-dependent, stronger-in-males description to all four findings. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • In the Tg-FDD;Mapt−/− model, oligodendrocyte function was restored to WT levels following tau ablation.

    “In the Tg-FDD;Mapt−/− model, we previously showed that oligodendrocyte function was restored to WT levels following tau ablation [85].”

    From Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease (2026) · cites this paper as [85]

    In the Results section on oligodendrocyte function (page unavailable), the paper says tau reduction recovered oligodendrocyte-related gene-expression alterations to wild-type levels. Its Discussion describes oligodendrocyte dysfunction as mitigated, but the cited evidence is gene expression, not a demonstration that oligodendrocyte function itself was fully restored to wild-type levels. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Tau ablation is beneficial in a mouse model of cerebral amyloid angiopathy (CAA), reducing vascular damage and improving behavioral outcomes.

    “Moreover, we recently demonstrated that tau ablation is beneficial in a mouse model of cerebral amyloid angiopathy (CAA), reducing vascular damage and improving behavioral outcomes [85].”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 60

  1. [1]Attems J. Sporadic cerebral amyloid angiopathy: pathology, clinical implications, and possible pathomechanisms. Acta Neuropathol. 2005; 110(4): 345‐ 359. doi: 10.1007/s00401-005-1074-9 16170565 · DOI · Paper page
  2. [2]Biffi A, Greenberg SM. Cerebral Amyloid Angiopathy: A Systematic Review. J Clin Neurol. 2011; 7(1): 1. doi: 10.3988/jcn.2011.7.1.1 21519520 PMC3079153 · DOI
  3. [3]Cisternas P, Taylor X, Lasagna‐Reeves CA. The Amyloid‐Tau‐Neuroinflammation Axis in the Context of Cerebral Amyloid Angiopathy. IJMS. 2019; 20(24): 6319. doi: 10.3390/ijms20246319 31847365 PMC6941131 · DOI
  4. [4]Garringer HJ, Murrell J, D'Adamio L, Ghetti B, Vidal R. Modeling familial British and Danish dementia. Brain Struct Funct. 2010; 214(2‐3): 235‐ 244. doi: 10.1007/s00429-009-0221-9 19779737 PMC8375673 · DOI
  5. [6]Vidal R, Frangione B, Rostagno A, et al. A stop‐codon mutation in the BRI gene associated with familial British dementia. Nature. 1999; 399(6738): 776‐ 781. doi: 10.1038/21637 10391242 · DOI · Paper page
  6. [7]Ghetti B, Perinit F, Kitamotoii T, et al. Vascular variant of prion protein cerebral amyloidosis with 7‐positive neurofibrillary tangles: The phenotype of the stop codon 145 mutation in PRNP. Proc Natl Acad Sci USA. Published online 1996. PMC40125 8570627
  7. [8]Vidal R, Calero M, Piccardo P, et al. Senile dementia associated with amyloid ‚ protein angiopathy and tau perivascular pathology but not neuritic plaques in patients homozygous for the APOE‐ε4 allele. Published online 2000. 10912914
  8. [9]Oshima K, Uchikado H, Dickson DW. Perivascular Neuritic Dystrophy Associated with Cerebral Amyloid Angiopathy in Alzheimer's Disease. Published online 2008. PMC2480573 18787622
  9. [10]Schoemaker D, Charidimou A, Zotin MCZ, et al. Memory impairment is a clinical marker of tau pathology in cerebral amyloid angiopathy: Neuroimaging /differential diagnosis. Alzheimers Dement. 2020; 16(S4): e037524. doi: 10.1002/alz.037524 · DOI
  10. [11]Rabin JS, Nichols E, La Joie R, et al. Cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline. Brain. 2022; 145(8): 2823‐ 2833. doi: 10.1093/brain/awac178 35759327 PMC9420012 · DOI
  11. [12]Hoglund Z, Ruiz‐Uribe N, Del Sastre E, et al. Brain vasculature accumulates tau and is spatially related to tau tangle pathology in Alzheimer's disease. Acta Neuropathol. 2024; 147(1): 101. doi: 10.1007/s00401-024-02751-9 38884806 PMC11182845 · DOI
  12. [13]Roberson ED, Scearce‐Levie K, Palop JJ, et al. Reducing Endogenous Tau Ameliorates Amyloid ß‐Induced Deficits in an Alzheimer's Disease Mouse Model. Science. 2007; 316(5825): 750‐ 754. doi: 10.1126/science.1141736 17478722 · DOI · Paper page
  13. [14]Roberson ED, Halabisky B, Yoo JW, et al. Amyloid‐β/Fyn–Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer's Disease. J Neurosci. 2011; 31(2): 700‐ 711. doi: 10.1523/JNEUROSCI.4152-10.2011 21228179 PMC3325794 · DOI · Paper page
  14. [15]Fernández‐Nogales M, Cabrera JR, Santos‐Galindo M, et al. Huntington's disease is a four‐repeat tauopathy with tau nuclear rods. Nat Med. 2014; 20(8): 881‐ 885. doi: 10.1038/nm.3617 25038828 · DOI · Paper page
  15. [16]Singh B, Covelo A, Martell‐Martínez H, et al. Tau is required for progressive synaptic and memory deficits in a transgenic mouse model of α‐synucleinopathy. Acta Neuropathol. 2019; 138(4): 551‐ 574. doi: 10.1007/s00401-019-02032-w 31168644 PMC6778173 · DOI
  16. [18]Blair LJ, Frauen HD, Zhang B, et al. Tau depletion prevents progressive blood‐brain barrier damage in a mouse model of tauopathy. Acta Neuropathol Commun. 2015; 3(1): 8. doi: 10.1186/s40478-015-0186-2 25775028 PMC4353464 · DOI · Paper page
  17. [19]Faraco G, Hochrainer K, Segarra SG, et al. Dietary salt promotes cognitive impairment through tau phosphorylation. Nature. 2019; 574(7780): 686‐ 690. doi: 10.1038/s41586-019-1688-z 31645758 PMC7380655 · DOI · Paper page
  18. [21]Taylor X, Cisternas P, Jury N, et al. Activated endothelial cells induce a distinct type of astrocytic reactivity. Commun Biol. 2022; 5(1): 282. doi: 10.1038/s42003-022-03237-8 35351973 PMC8964703 · DOI
  19. [22]Vidal R, Barbeito AG, Miravalle L, Ghetti B. Cerebral Amyloid Angiopathy and Parenchymal Amyloid Deposition in Transgenic Mice Expressing the Danish Mutant Form of Human BRI 2. Brain Pathology. 2009; 19(1): 58‐ 68. doi: 10.1111/j.1750-3639.2008.00164.x 18410407 PMC2605177 · DOI · Paper page
  20. [23]Cisternas P, Taylor X, Perkins A, et al. Vascular amyloid accumulation alters the gabaergic synapse and induces hyperactivity in a model of cerebral amyloid angiopathy. Aging Cell. 2020; 19(10): e13233. doi: 10.1111/acel.13233 32914559 PMC7576303 · DOI
  21. [24]Patel H, Martinez P, Perkins A, et al. Pathological tau and reactive astrogliosis are associated with distinct functional deficits in a mouse model of tauopathy. Neurobiology of Aging. 2022; 109: 52‐ 63. doi: 10.1016/j.neurobiolaging.2021.09.006 34655981 PMC8671336 · DOI
  22. [26]Cisternas P, Taylor X, Martinez P, Maldonado O, Jury N, Lasagna‐Reeves CA. The reduction of astrocytic tau prevents amyloid‐β‐induced synaptotoxicity. Brain Communications. 2022; 4(5): fcac235. doi: 10.1093/braincomms/fcac235 36196088 PMC9527666 · DOI
  23. [27]Puzzo D, Argyrousi EK, Staniszewski A, et al. Tau is not necessary for amyloid‐β–induced synaptic and memory impairments. Journal of Clinical Investigation. 2020; 130(9): 4831‐ 4844. doi: 10.1172/JCI137040 32544084 PMC7456211 · DOI
  24. [28]Petersen MA, Ryu JK, Akassoglou K. Fibrinogen in neurological diseases: mechanisms, imaging and therapeutics. Nat Rev Neurosci. 2018; 19(5): 283‐ 301. doi: 10.1038/nrn.2018.13 29618808 PMC6743980 · DOI · Paper page
  25. [29]Taylor X, Cisternas P, You Y, et al. A1 reactive astrocytes and a loss of TREM2 are associated with an early stage of pathology in a mouse model of cerebral amyloid angiopathy. J Neuroinflammation. 2020; 17(1): 223. doi: 10.1186/s12974-020-01900-7 32711525 PMC7382050 · DOI
  26. [31]Laske C, Stellos K, Stransky E, Leyhe T, Gawaz M. Decreased Plasma Levels of Granulocyte‐Colony Stimulating Factor (G‐CSF) in Patients with Early Alzheimer's Disease. Journal of Alzheimer's Disease. 2009; 17(1): 115‐ 123. doi: 10.3233/JAD-2009-1017 19494436 · DOI
  27. [32]Prakash A, Medhi B, Chopra K. Granulocyte colony stimulating factor (GCSF) improves memory and neurobehavior in an amyloid‐β induced experimental model of Alzheimer's disease. Pharmacology Biochemistry and Behavior. 2013; 110: 46‐ 57. doi: 10.1016/j.pbb.2013.05.015 23756182 · DOI
  28. [33]Wang SM, Kang DW, Kim HJ, Park SS, Lim HK. Neuroplastic and Pro‐cognitive Effects of Granulocyte Colony Stimulating Factor in Healthy Adults: A Pilot Study. Psychiatry Investig. 2023; 20(10): 984‐ 990. doi: 10.30773/pi.2023.0150 PMC10620331 37899222 · DOI
  29. [34]Litvinchuk A, Wan YW, Swartzlander DB, et al. Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer's Disease. Neuron. 2018; 100(6): 1337‐ 1353.e5. doi: 10.1016/j.neuron.2018.10.031 30415998 PMC6309202 · DOI · Paper page
  30. [35]Propson NE, Roy ER, Litvinchuk A, Köhl J, Zheng H. Endothelial C3a receptor mediates vascular inflammation and blood‐brain barrier permeability during aging. Journal of Clinical Investigation. 2021; 131(1): e140966. doi: 10.1172/JCI140966 32990682 PMC7773352 · DOI · Paper page
  31. [36]Kaji S, Maki T, Ueda J, et al. BCAS1‐positive immature oligodendrocytes are affected by the α‐synuclein‐induced pathology of multiple system atrophy. acta neuropathol commun. 2020; 8(1): 120. doi: 10.1186/s40478-020-00997-4 32727582 PMC7391509 · DOI · Paper page
  32. [37]Morita J, Kano K, Kato K, et al. Structure and biological function of ENPP6, a choline‐specific glycerophosphodiester‐phosphodiesterase. Sci Rep. 2016; 6(1): 20995. doi: 10.1038/srep20995 26888014 PMC4757880 · DOI
  33. [38]Patyal P, Fil D, Wight PA. Plp1 in the enteric nervous system is preferentially expressed during early postnatal development in mouse as DM20, whose expression appears reliant on an intronic enhancer. Front Cell Neurosci. 2023; 17: 1175614. doi: 10.3389/fncel.2023.1175614 37293625 PMC10244531 · DOI
  34. [39]Teng XY, Hu P, Zhang CM, et al. OPALIN is an LGI1 receptor promoting oligodendrocyte differentiation. Proceedings of the National Academy of Sciences. 2024; 121(32): e2403652121. doi: 10.1073/pnas.2403652121 PMC11317624 39083419 · DOI
  35. [40]Pak K, Chan SL, Mattson MP. Presenilin‐1 mutation sensitizes oligodendrocytes to glutamate and amyloid toxicities, and exacerbates white matter damage and memory impairment in mice. Neuromol Med. 2003; 3(1): 53‐ 64. doi: 10.1385/NMM:3:1:53 12665676 · DOI
  36. [41]Behrendt G, Baer K, Buffo A, et al. Dynamic changes in myelin aberrations and oligodendrocyte generation in chronic amyloidosis in mice and men. Glia. 2013; 61(2): 273‐ 286. doi: 10.1002/glia.22432 23090919 · DOI · Paper page
  37. [42]Desai MK, Sudol KL, Janelsins MC, Mastrangelo MA, Frazer ME, Bowers WJ. Triple‐transgenic Alzheimer's disease mice exhibit region‐specific abnormalities in brain myelination patterns prior to appearance of amyloid and tau pathology. Glia. 2009; 57(1): 54‐ 65. doi: 10.1002/glia.20734 18661556 PMC2584762 · DOI · Paper page
  38. [43]Xu J, Chen S, Ahmed SH, et al. Amyloid‐β Peptides Are Cytotoxic to Oligodendrocytes. J Neurosci. 2001; 21(1): RC118‐ RC118. doi: 10.1523/JNEUROSCI.21-01-j0001.2001 11150354 PMC6762453 · DOI · Paper page
  39. [44]Mummery CJ, Börjesson‐Hanson A, Blackburn DJ, et al. Tau‐targeting antisense oligonucleotide MAPTRx in mild Alzheimer's disease: a phase 1b, randomized, placebo‐controlled trial. Nat Med. 2023; 29(6): 1437‐ 1447. doi: 10.1038/s41591-023-02326-3 37095250 PMC10287562 · DOI · Paper page
  40. [45]Sin MK, Zamrini E, Ahmed A, Nho K, Hajjar I. Anti‐Amyloid Therapy, AD, and ARIA: Untangling the Role of CAA. J Clin Med. 2023; 12(21): 6792. doi: 10.3390/jcm12216792 37959255 PMC10647766 · DOI
  41. [46]Nation DA, Edmonds EC, Bangen KJ, et al. Pulse Pressure in Relation to Tau‐Mediated Neurodegeneration, Cerebral Amyloidosis, and Progression to Dementia in Very Old Adults. JAMA Neurol. 2015; 72(5): 546. doi: 10.1001/jamaneurol.2014.4477 25822631 PMC4428938 · DOI
  42. [47]Kim HJ, Park S, Cho H, et al. Assessment of Extent and Role of Tau in Subcortical Vascular Cognitive Impairment Using 18F‐AV1451 Positron Emission Tomography Imaging. JAMA Neurol. 2018; 75(8): 999‐ 1007. doi: 10.1001/jamaneurol.2018.0975 29799981 PMC6142932 · DOI
  43. [48]Selkoe DJ, Hardy J. The amyloid hypothesis of Alzheimer's disease at 25 years. EMBO Mol Med. 2016; 8(6): 595‐ 608. doi: 10.15252/emmm.201606210 27025652 PMC4888851 · DOI · Paper page
  44. [49]Hawkes CA, Härtig W, Kacza J, et al. Perivascular drainage of solutes is impaired in the ageing mouse brain and in the presence of cerebral amyloid angiopathy. Acta Neuropathol. 2011; 121(4): 431‐ 443. doi: 10.1007/s00401-011-0801-7 21259015 · DOI
  45. [50]Arbel‐Ornath M, Hudry E, Eikermann‐Haerter K, et al. Interstitial fluid drainage is impaired in ischemic stroke and Alzheimer's disease mouse models. Acta Neuropathol. 2013; 126(3): 353‐ 364. doi: 10.1007/s00401-013-1145-2 23818064 PMC3810119 · DOI
  46. [52]Merlini M, Rafalski VA, Rios Coronado PE, et al. Fibrinogen Induces Microglia‐Mediated Spine Elimination and Cognitive Impairment in an Alzheimer's Disease Model. Neuron. 2019; 101(6): 1099‐ 1108.e6. doi: 10.1016/j.neuron.2019.01.014 30737131 PMC6602536 · DOI · Paper page
  47. [53]Shinohara M, Murray ME, Frank RD, et al. Impact of sex and APOE4 on cerebral amyloid angiopathy in Alzheimer's disease. Acta Neuropathol. 2016; 132(2): 225‐ 234. doi: 10.1007/s00401-016-1580-y 27179972 PMC4947445 · DOI · Paper page
  48. [54]Aggarwal NT, Mielke MM. Sex Differences in Alzheimer's Disease. Neurologic Clinics. 2023; 41(2): 343‐ 358. doi: 10.1016/j.ncl.2023.01.001 37030962 PMC10321561 · DOI
  49. [55]Cipolla MJ, Godfrey JA, Wiegman MJ. The Effect of Ovariectomy and Estrogen on Penetrating Brain Arterioles and Blood‐Brain Barrier Permeability. Microcirculation. 2009; 16(8): 685‐ 693. doi: 10.3109/10739680903164131 19905968 PMC2857914 · DOI
  50. [56]Wilson AC, Clemente L, Liu T, Bowen RL, Meethal SV, Atwood CS. Reproductive hormones regulate the selective permeability of the blood‐brain barrier. Biochimica et Biophysica Acta (BBA) ‐ Molecular Basis of Disease. 2008; 1782(6): 401‐ 407. doi: 10.1016/j.bbadis.2008.02.011 18381207 · DOI
  51. [57]Parrado‐Fernández C, Blennow K, Hansson M, Leoni V, Cedazo‐Minguez A, Björkhem I. Evidence for sex difference in the csf /plasma albumin ratio in ∼20 000 patients and 335 healthy volunteers. J Cellular Molecular Medi. 2018; 22(10): 5151‐ 5154. doi: 10.1111/jcmm.13767 PMC6156389 30054982 · DOI
  52. [59]Rapoport M, Dawson HN, Binder LI, Vitek MP, Ferreira A. Tau is essential to β‐amyloid‐induced neurotoxicity. Proceedings of the National Academy of Sciences. 2002; 99(9): 6364‐ 6369. doi: 10.1073/pnas.092136199 PMC122954 11959919 · DOI · Paper page
  53. [60]Tai C, Chang CW, Yu GQ, et al. Tau Reduction Prevents Key Features of Autism in Mouse Models. Neuron. 2020; 106(3): 421‐ 437.e11. doi: 10.1016/j.neuron.2020.01.038 32126198 PMC7210056 · DOI · Paper page
  54. [61]Das M, Mao W, Shao E, et al. Interdependence of neural network dysfunction and microglial alterations in Alzheimer's disease‐related models. iScience. 2021; 24(11): 103245. doi: 10.1016/j.isci.2021.103245 34755090 PMC8561005 · DOI · Paper page
  55. [63]Eyo UB, Murugan M, Wu L. Microglia–Neuron Communication in Epilepsy. Glia. 2017; 65(1): 5‐ 18. doi: 10.1002/glia.23006 27189853 PMC5116010 · DOI
  56. [65]Ezerskiy LA, Schoch KM, Sato C, et al. Astrocytic 4R tau expression drives astrocyte reactivity and dysfunction. JCI Insight. 7(1): e152012. doi: 10.1172/jci.insight.152012 PMC8765054 34874917 · DOI
  57. [66]Goodman LD, Ralhan I, Li X, et al. Tau is required for glial lipid droplet formation and resistance to neuronal oxidative stress. Nat Neurosci. 2024; 27(10): 1918‐ 1933. doi: 10.1038/s41593-024-01740-1 39187706 PMC11809452 · DOI
  58. [67]Desai MK, Guercio BJ, Narrow WC, Bowers WJ. An Alzheimer's Disease‐relevant Presenilin‐1 Mutation Augments Amyloid‐beta‐induced Oligodendrocyte Dysfunction. Glia. 2011; 59(4): 627‐ 640. doi: 10.1002/glia.21131 21294162 PMC3045399 · DOI
  59. [68]Sims R, Hollingworth P, Moskvina V, et al. Evidence that variation in the oligodendrocyte lineage transcription factor 2 (OLIG2) gene is associated with psychosis in Alzheimer's disease. Neurosci Lett. 2009; 461(1): 54‐ 59. doi: 10.1016/j.neulet.2009.05.051 19477230 · DOI
  60. [69]Torii T, Miyamoto Y, Nakata R, et al. Identification of Tau protein as a novel marker for maturation and pathological changes of oligodendrocytes. Glia. 2023; 71(4): 1002‐ 1017. doi: 10.1002/glia.24322 36565228 · DOI

Cited by

Sorted by citations

Authors
Jury‐Garfe, N., Chimal‐Juárez, E., Patel, H., Martinez‐Pinto, J., Vanderbosch, K., Mardones, M. D., Perkins, A., Prisco, G. V. D., Marambio, Y., Vidal, R., Atwood, B. K., & Lasagna‐Reeves, C. A.
Affiliations
  • Stark Neurosciences Research Institute Indiana University School of Medicine Indianapolis Indiana USA
  • Indiana University Indianapolis (US)
  • Baylor College of Medicine (US)
  • University of Minnesota (US)
Corresponding author
Lasagna‐Reeves, Cristian A.
Venue
Alzheimer's & Dementia
Publisher
Wiley
Published
2025-05
Volume
21
Issue
5
Pages
e70238-e70238
ISSN
  • 1552-5260 (ISSN-L)
  • 1552-5279
OpenAlex
W4410220417
Cited by
5
References
9
Citations by year
2026: 4 · 2025: 1
FWCI
3.22
Type
journal article
Language
en
Open access
Locations
  • Alzheimer s & Dementia (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • IUScholarWorks (Indiana University) (submittedVersion, cc-by-nc-nd)
  • Digital Commons-TMC (Texas Medical Center) (submittedVersion)
Funders
  • Alzheimer's Association (ALZDISCOVERY‐1049108)
  • Cure Alzheimer's Fund
  • Rainwater Charitable Foundation
  • Indiana Clinical and Translational Sciences Institute (UL1TR002529)
  • National Center for Advancing Translational Sciences
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
MeSH terms
Animals, Brain, Disease Models, Animal, Mice, Transgenic, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, tau Proteins, Mice, Knockout, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review