Alzheimer’s Association. 2020 Alzheimer’s illness realities and figures. Alzheimers Dement. 16, 391–460 (2020).
Sengupta, U. & Kayed, R. Amyloid β, tau, and α-synuclein aggregates in the pathogenesis, diagnosis, and rehabs for neurodegenerative illness. Prog. Neurobiol. 214, 102270 (2022).
Jellinger, K. A. & Attems, J. Challenges of multimorbidity of the aging brain: a crucial update. J. Neural Transm. 122, 505–521 (2015).
Tanne, J. H. Aduhelm: approval of Alzheimer’s drug was extremely unconventional, discovers report. BMJ 380, 6 (2023).
van Dyck, C. H. et al. Lecanemab in early Alzheimer’s illness. N. Engl. J. Med. 388, 9–21 (2023).
Perry, R. J. & Hodges, J. R. Attention and executive deficits in Alzheimer’s illness. A critique. Brain 122, 383–404 (1999).
Polanco, J. C. et al. Amyloid-β and tau intricacy—towards enhanced biomarkers and targeted treatments. Nat. Rev. Neurol. 14, 22–39 (2018).
Götz, J. & Ittner, L. M. Animal designs of Alzheimer’s illness and frontotemporal dementia. Nat. Rev. Neurosci. 9, 532–544 (2008).
Dujardin, S., Colin, M. & Buee, L. Invited evaluation: animal designs of tauopathies and their ramifications for research/translation into the center. Neuropathol. Appl. Neurobiol. 41, 59–80 (2015).
Jankowsky, J. L. & Zheng, H. Practical factors to consider for picking a mouse design of Alzheimer’s illness. Mol. Neurodegener. 12, 89 (2017).
Schenk, D. et al. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature 400, 173–177 (1999).
Bard, F. et al. Peripherally administered antibodies versus amyloid β-peptide get in the main nerve system and minimize pathology in a mouse design of Alzheimer illness. Nat. Med. 6, 916–919 (2000).
de la Torre, J. C. & Mussivand, T. Can disrupted brain microcirculation cause Alzheimer’s illness? Neurol. Res. 15, 146–153 (1993).
Grimm, A. & Eckert, A. Brain aging and neurodegeneration: from a mitochondrial perspective. J. Neurochem. 143, 418–431 (2017).
Heneka, M. T. et al. Neuroinflammation in Alzheimer’s illness. Lancet Neurol. 14, 388–405 (2015).
Wirths, O. & Zampar, S. Neuron loss in Alzheimer’s illness: translation in transgenic mouse designs. Int. J. Mol. Sci. 21, 8144 (2020).
Eimer, W. A. & Vassar, R. Neuron loss in the 5XFAD mouse design of Alzheimer’s illness associates with intraneuronal Aβ42 build-up and caspase-3 activation. Mol. Neurodegener. 8, 2 (2013).
van Eersel, J. et al. Early-start axonal pathology in an unique P301S-tau transgenic mouse design of frontotemporal lobar degeneration. Neuropathol. Appl. Neurobiol. 41, 906–925 (2015).
Hatch, R. J., Wei, Y., Xia, D. & Götz, J. Hyperphosphorylated tau triggers decreased hippocampal CA1 excitability by transferring the axon preliminary sector. Acta Neuropathol. 133, 717–730 (2017).
Roy, D. S. et al. Memory retrieval by triggering engram cells in mouse designs of early Alzheimer’s illness. Nature 531, 508–512 (2016).
Oh, H., Razlighi, Q. R. & Stern, Y. Multiple paths of reserve all at once present in cognitively regular older grownups. Neurology 90, e197–e205 (2018).
Stern, Y., Barnes, C. A., Grady, C., Jones, R. N. & Raz, N. Brain reserve, cognitive reserve, payment, and upkeep: operationalization, credibility, and systems of cognitive strength. Neurobiol. Aging 83, 124–129 (2019).
Ammassari-Teule, M. Neural payment in presymptomatic hAPP mouse designs of Alzheimer’s illness. Learn. Mem. 27, 390–394 (2020).
Morrone, C. D., Lai, A. Y., Bishay, J., Hill, M. E. & McLaurin, J. Parvalbumin neuroplasticity makes up for somatostatin problems, preserving cognitive function in Alzheimer’s illness. Transl. Neurodegener. 11, 26 (2022).
Probst, A. et al. Axonopathy and amyotrophy in mice transgenic for human four-repeat tau protein. Acta Neuropathol. 99, 469–481 (2000).
Allen, B. et al. Abundant tau filaments and nonapoptotic neurodegeneration in transgenic mice revealing human P301S tau protein. J. Neurosci. 22, 9340–9351 (2002).
Santacruz, K. et al. Tau suppression in a neurodegenerative mouse design enhances memory function. Science 309, 476–481 (2005).
Götz, J., Bodea, L. G. & Goedert, M. Rodent designs for Alzheimer illness. Nat. Rev. Neurosci. 19, 583–598 (2018).
Saito, T. et al. Single App knock-in mouse designs of Alzheimer’s illness. Nat. Neurosci. 17, 661–663 (2014).
Sato, K. et al. A third-generation mouse design of Alzheimer’s illness reveals early and increased cored plaque pathology made up of wild-type human amyloid β peptide. J. Biol. Chem. 297, 101004 (2021).
Xia, D., Gutmann, J. M. & Götz, J. Mobility and subcellular localization of endogenous, gene-edited tau varies from that of over-expressed human wild-type and P301L mutant tau. Sci. Rep. 6, 29074 (2016).
Bjorkhem, I. et al. Cholesterol homeostasis in human brain: turnover of 24S-hydroxycholesterol and proof for a cerebral origin of the majority of this oxysterol in the flow. J. Lipid Res. 39, 1594–1600 (1998).
Huynh, T. V. et al. Lack of hepatic ApoE does not affect early Aβ deposition: observations from a brand-new APOE knock-in design. Mol. Neurodegener. 14, 37 (2019).
Barisano, G. et al. A ‘multi-omics’ analysis of blood–brain barrier and synaptic dysfunction in APOE4 mice. J. Exp. Med. 219, e20221137 (2022).
Shi, Y. et al. ApoE4 significantly intensifies tau-mediated neurodegeneration in a mouse design of tauopathy. Nature 549, 523–527 (2017).
Bales, K. R. et al. Human APOE isoform-dependent impacts on brain β-amyloid levels in PDAPP transgenic mice. J. Neurosci. 29, 6771–6779 (2009).
Castellano, J. M. et al. Human ApoE isoforms differentially control brain amyloid-β peptide clearance. Sci. Transl. Med. 3, 89ra57 (2011).
Hou, J., Chen, Y., Grajales-Reyes, G. & Colonna, M. TREM2 reliant and independent functions of microglia in Alzheimer’s illness. Mol. Neurodegener. 17, 84 (2022).
Fitz, N. F. et al. Trem2 shortage differentially impacts phenotype and transcriptome of human APOE3 and APOE4 mice. Mol. Neurodegener. 15, 41 (2020).
Humpel, C. Organotypic brain piece cultures: an evaluation. Neuroscience 305, 86–98 (2015).
Fath, T., Ke, Y. D., Gunning, P., Götz, J. & Ittner, L. M. Primary assistance cultures of hippocampal and substantia nigra nerve cells. Nat. Protoc. 4, 78–85 (2009).
Pir, G. J., Choudhary, B. & Mandelkow, E. Caenorhabditis elegans designs of tauopathy. FASEB J. 31, 5137–5148 (2017).
Griffin, E. F., Caldwell, K. A. & Caldwell, G. A. Genetic and medicinal discovery for Alzheimer’s illness utilizing Caenorhabditis elegans. AIR CONDITIONER Chem. Neurosci. 8, 2596–2606 (2017).
Asadzadeh, J. et al. Retromer shortage in tauopathy designs boosts the truncation and toxicity of tau. Nat. Commun. 13, 5049 (2022).
Saleem, S. & Kannan, R. R. Zebrafish: an emerging real-time design system to research study Alzheimer’s illness and neurospecific drug discovery. Cell Death Discov. 4, 45 (2018).
Pang, K. et al. An App knock-in rat design for Alzheimer’s illness displaying Aβ and tau pathologies, neuronal death and cognitive problems. Cell Res. 32, 157–175 (2022).
Hurley, M. J. et al. Genome sequencing variations in the Octodon degus, a non-traditional natural design of aging and Alzheimer’s illness. Front. Aging Neurosci. 14, 894994 (2022).
Reid, S. J. et al. Alzheimer’s illness markers in the aged sheep (Ovis aries). Neurobiol. Aging 58, 112–119 (2017).
Yan, S. et al. A huntingtin knockin pig design recapitulates functions of selective neurodegeneration in Huntington’s illness. Cell 173, 989–1002 (2018).
Lee, S. E. et al. Production of transgenic pig as an Alzheimer’s illness design utilizing a multi-cistronic vector system. PLoS ONE 12, e0177933 (2017).
Walker, L. C. & Jucker, M. The remarkable vulnerability of human beings to Alzheimer’s illness. Trends Mol. Med. 23, 534–545 (2017).
Haque, R. U. & Levey, A. I. Alzheimer’s illness: a scientific viewpoint and future nonhuman primate research study opportunities. Proc. Natl Acad. Sci. U.S.A. 116, 26224–26229 (2019).
Paspalas, C. D. et al. The aged rhesus macaque manifests Braak phase III/IV Alzheimer’s-like pathology. Alzheimers Dement. 14, 680–691 (2018).
Sasaguri, H. et al. Recent advances in the modeling of Alzheimer’s illness. Front. Neurosci. 16, 807473 (2022).
Yoshimatsu, S. et al. Multimodal analyses of a non-human primate design harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter. Neurosci. Res. 185, 49–61 (2022).
Seita, Y. et al. Generation of transgenic cynomolgus monkeys overexpressing the gene for amyloid-β precursor protein. J. Alzheimers Dis. 75, 45–60 (2020).
Tang, M. et al. Neurological symptoms of autosomal dominant familial Alzheimer’s illness: a contrast of the released literature with the Dominantly Inherited Alzheimer Network observational research study (DIAN-OBS). Lancet Neurol. 15, 1317–1325 (2016).
Lear, A. et al. Understanding them to comprehend ourselves: the value of NHP research study for translational neuroscience. Curr. Res. Neurobiol. 3, 100049 (2022).
Kennedy, M. E. et al. The BACE1 inhibitor verubecestat (MK-8931) decreases CNS β-amyloid in animal designs and in Alzheimer’s illness clients. Sci. Transl. Med. 8, 363ra150 (2016).
Amin, N. D. & Pasca, S. P. Building designs of brain conditions with three-dimensional organoids. Neuron 100, 389–405 (2018).
Park, J. et al. A 3D human triculture system modeling neurodegeneration and neuroinflammation in Alzheimer’s illness. Nat. Neurosci. 21, 941–951 (2018).
Fair, S. R. et al. Electrophysiological maturation of cerebral organoids associates with vibrant morphological and cellular advancement. Stem Cell Rep. 15, 855–868 (2020).
Sun, X. Y. et al. Generation of vascularized brain organoids to study neurovascular interactions. eLife 11, e76707 (2022).
Shin, N. et al. Vascularization of iNSC spheroid in a 3D spheroid-on-a-chip platform boosts neural maturation. Biotechnol. Bioeng. 119, 566–574 (2022).
Duque, A., Arellano, J. I. & Rakic, P. An evaluation of the presence of adult neurogenesis in human beings and worth of its rodent designs for neuropsychiatric illness. Mol. Psychiatry 27, 377–382 (2022).
Sloan, S. A. et al. Human astrocyte maturation recorded in 3D cerebral cortical spheroids stemmed from pluripotent stem cells. Neuron 95, 779–790 (2017).
Lopez-Otin, C. & Kroemer, G. Hallmarks of health. Cell 184, 33–63 (2021).
Lopez-Otin, C., Blasco, M. A., Partridge, L., Serrano, M. & Kroemer, G. Hallmarks of aging: a broadening universe. Cell 186, 243–278 (2022).
Turturro, A., Duffy, P., Hass, B., Kodell, R. & Hart, R. Survival attributes and age-adjusted illness occurrences in C57BL/6 mice fed a typically utilized cereal-based diet plan regulated by dietary limitation. J. Gerontol. A Biol. Sci. Med. Sci. 57, B379–B389 (2002).
Blackmore, D. G. et al. Multimodal analysis of aged wild-type mice exposed to duplicated scanning ultrasound treatments shows long-lasting safety. Theranostics 8, 6233–6247 (2018).
van Praag, H., Shubert, T., Zhao, C. & Gage, F. H. Exercise boosts knowing and hippocampal neurogenesis in aged mice. J. Neurosci. 25, 8680–8685 (2005).
Blackmore, D. G. et al. Low-strength ultrasound brings back long-lasting potentiation and memory in senescent mice through pleiotropic systems consisting of NMDAR signaling. Mol. Psychiatry 26, 6975–6991 (2021).
Nisbet, R. M. et al. Combined impacts of scanning ultrasound and a tau-specific single chain antibody in a tau transgenic mouse design. Brain 140, 1220–1230 (2017).
Pandit, R., Leinenga, G. & Götz, J. Repeated ultrasound treatment of tau transgenic mice clears neuronal tau by autophagy and enhances behavioral functions. Theranostics 9, 3754–3767 (2019).
Xu, G. et al. Using the capacity of inducible tau/APP transgenic mice. Neuropathol. Appl. Neurobiol. 48, e12791 (2022).
Beckmann, N., Gerard, C., Abramowski, D., Cannet, C. & Staufenbiel, M. Noninvasive magnetic resonance imaging detection of cerebral amyloid angiopathy-related microvascular changes utilizing superparamagnetic iron oxide particles in APP transgenic mouse designs of Alzheimer’s illness: application to passive Aβ immunotherapy. J. Neurosci. 31, 1023–1031 (2011).
Lewis, J. et al. Neurofibrillary tangles, amyotrophy and progressive motor disruption in mice revealing mutant (P301L) tau protein. Nat. Genet. 25, 402–405 (2000).
Coninx, E. et al. Hippocampal and cortical tissue-specific epigenetic clocks suggest an increased epigenetic age in a mouse design for Alzheimer’s illness. Aging 12, 20817–20834 (2020).
Gamache, J. et al. Factors aside from hTau overexpression that add to tauopathy-like phenotype in rTg4510 mice. Nat. Commun. 10, 2479 (2019).
Polanco, J. C., Hand, G. R., Briner, A., Li, C. & Götz, J. Exosomes cause endolysosomal permeabilization as an entrance by which exosomal tau seeds leave into the cytosol. Acta Neuropathol. 141, 235–256 (2021).
Thal, D. R. et al. Estimation of amyloid circulation by [18F]flutemetamol animal forecasts the neuropathological stage of amyloid β-protein deposition. Acta Neuropathol. 136, 557–567 (2018).
Braak, H. & Braak, E. Staging of Alzheimer’s disease-related neurofibrillary modifications. Neurobiol. Aging 16, 271–278 (1995).
Jucker, M. & Walker, L. C. Self-proliferation of pathogenic protein aggregates in neurodegenerative illness. Nature 501, 45–51 (2013).
de Calignon, A. et al. Propagation of tau pathology in a design of early Alzheimer’s illness. Neuron 73, 685–697 (2012).
Asai, H. et al. Depletion of microglia and inhibition of exosome synthesis stop tau proliferation. Nat. Neurosci. 18, 1584–1593 (2015).
Clavaguera, F. et al. Brain homogenates from human tauopathies cause tau additions in mouse brain. Proc. Natl Acad. Sci. U.S.A. 110, 9535–9540 (2013).
Ahmed, Z. et al. An unique in vivo design of tau proliferation with quick and progressive neurofibrillary tangle pathology: the pattern of spread is identified by connection, not distance. Acta Neuropathol. 127, 667–683 (2014).
Ferris, S. H. et al. Positron emission tomography in the research study of aging and senile dementia. Neurobiol. Aging 1, 127–131 (1980).
Palop, J. J. & Mucke, L. Network irregularities and interneuron dysfunction in Alzheimer illness. Nat. Rev. Neurosci. 17, 777–792 (2016).
Sheline, Y. I. et al. APOE4 allele interrupts resting state fMRI connection in the lack of amyloid plaques or reduced CSF Aβ42. J. Neurosci. 30, 17035–17040 (2010).
Palmqvist, S. et al. Earliest build-up of β-amyloid happens within the default-mode network and simultaneously impacts brain connection. Nat. Commun. 8, 1214 (2017).
Zott, B., Busche, M. A., Sperling, R. A. & Konnerth, A. What occurs with the circuit in Alzheimer’s illness in mice and human beings? Annu. Rev. Neurosci. 41, 277–297 (2018).
Lu, H. et al. Rat brains likewise have a default mode network. Proc. Natl Acad. Sci. U.S.A. 109, 3979–3984 (2012).
Whitesell, J. D. et al. Regional, layer, and cell-type-specific connection of the mouse default mode network. Neuron 109, 545–559 (2021).
Zhou, Y. et al. Abnormal connection in the posterior cingulate and hippocampus in early Alzheimer’s illness and moderate cognitive problems. Alzheimers Dement. 4, 265–270 (2008).
Quiroz, Y. T. et al. Hippocampal hyperactivation in presymptomatic familial Alzheimer’s illness. Ann. Neurol. 68, 865–875 (2010).
O’Brien, J. L. et al. Longitudinal fMRI in elderly exposes loss of hippocampal activation with scientific decrease. Neurology 74, 1969–1976 (2010).
Busche, M. A. et al. Critical function of soluble amyloid-β for early hippocampal hyperactivity in a mouse design of Alzheimer’s illness. Proc. Natl Acad. Sci. U.S.A. 109, 8740–8745 (2012).
Palop, J. J. et al. Aberrant excitatory neuronal activity and countervailing improvement of repressive hippocampal circuits in mouse designs of Alzheimer’s illness. Neuron 55, 697–711 (2007).
Padmanabhan, P., Kneynsberg, A. & Götz, J. Super-resolution microscopy: a better take a look at synaptic dysfunction in Alzheimer illness. Nat. Rev. Neurosci. 22, 723–740 (2021).
Tzioras, M., McGeachan, R. I., Durrant, C. S. & Spires-Jones, T. L. Synaptic degeneration in Alzheimer illness. Nat. Rev. Neurol. 19, 19–38 (2023).
Sweeney, M. D., Zhao, Z., Montagne, A., Nelson, A. R. & Zlokovic, B. V. Blood–brain barrier: from physiology to illness and back. Physiol. Rev. 99, 21–78 (2019).
Pardridge, W. M. Tyrosine hydroxylase replacement in speculative Parkinson’s illness with transvascular gene treatment. NeuroRx 2, 129–138 (2005).
Neuwelt, E. et al. Strategies to advance translational research study into brain barriers. Lancet Neurol. 7, 84–96 (2008).
Golde, T. E. Open concerns for Alzheimer’s illness immunotherapy. Alzheimers Res. Ther. 6, 3 (2014).
Budd Haeberlein, S. et al. Two randomized stage 3 research studies of aducanumab in early Alzheimer’s illness. J. Prev. Alzheimers Dis. 9, 197–210 (2022).
Schneider, L. A resurrection of aducanumab for Alzheimer’s illness. Lancet Neurol. 19, 111–112 (2020).
Ayton, S. Ventricular augmentation brought on by aducanumab. Nat. Rev. Neurol. 18, 383–384 (2022).
Leinenga, G., Koh, W. K. & Götz, J. A relative research study of the impacts of aducanumab and scanning ultrasound on amyloid plaques and habits in the APP23 mouse design of Alzheimer illness. Alzheimers Res. Ther. 13, 76 (2021).
Sun, T. et al. Focused ultrasound with anti-pGlu3 Aβ boosts effectiveness in Alzheimer’s disease-like mice through recruitment of peripheral immune cells. J. Control. Release 336, 443–456 (2021).
Kovacs, Z. I. et al. Disrupting the blood–brain barrier by focused ultrasound causes sterilized swelling. Proc. Natl Acad. Sci. U.S.A. 114, E75–E84 (2017).
McMahon, D. & Hynynen, K. Acute inflammatory reaction following increased blood–brain barrier permeability caused by focused ultrasound depends on microbubble dosage. Theranostics 7, 3989–4000 (2017).
Clausznitzer, D. et al. Quantitative systems pharmacology design for Alzheimer illness shows targeting sphingolipid dysregulation as prospective treatment choice. CPT Pharmacometrics Syst. Pharmacol. 7, 759–770 (2018).
Madrasi, K. et al. Systematic in silico analysis of scientifically checked drugs for lowering amyloid-β plaque build-up in Alzheimer’s illness. Alzheimers Dement. 17, 1487–1498 (2021).
Vogel, J. W. et al. Four unique trajectories of tau deposition determined in Alzheimer’s illness. Nat. Med. 27, 871–881 (2021).
Cornblath, E. J. et al. Computational modeling of tau pathology spread exposes patterns of local vulnerability and the effect of a hereditary danger aspect. Sci. Adv. 7, eabg6677 (2021).
Meisl, G. et al. In vivo rate-determining actions of tau seed build-up in Alzheimer’s illness. Sci. Adv. 7, eabh1448 (2021).
Kunze, T., Hunold, A., Haueisen, J., Jirsa, V. & Spiegler, A. Transcranial direct existing stimulation modifications resting state practical connection: a massive brain network modeling research study. NeuroImage 140, 174–187 (2016).
Geerts, H. et al. A combined PBPK and QSP design for modeling amyloid aggregation in Alzheimer’s illness. CPT Pharmacometrics Syst. Pharmacol. (2023).
Taubes, A. et al. Experimental and real-world proof supporting the computational repurposing of bumetanide for APOE4-associated Alzheimer’s illness. Nat. Aging 1, 932–947 (2021).
Haeno, H. et al. Computational modeling of pancreatic cancer exposes kinetics of transition recommending maximum treatment methods. Cell 148, 362–375 (2012).
Padmanabhan, P., Desikan, R. & Dixit, N. M. Modeling how antibody reactions might figure out the effectiveness of COVID-19 vaccines. Nat. Comput. Sci. 2, 123–131 (2022).
Suberbielle, E. et al. Physiologic brain activity triggers DNA double-strand breaks in nerve cells, with worsening by amyloid-β. Nat. Neurosci. 16, 613–621 (2013).
Thadathil, N. et al. DNA double-strand break build-up in Alzheimer’s illness: proof from speculative designs and postmortem human brains. Mol. Neurobiol. 58, 118–131 (2021).
Rolyan, H. et al. Telomere reducing decreases Alzheimer’s illness amyloid pathology in mice. Brain 134, 2044–2056 (2011).
Shu, L. et al. Genome-large modification of 5-hydroxymenthylcytosine in a mouse design of Alzheimer’s illness. BMC Genomics 17, 381 (2016).
Cadena-del-Castillo, C. et al. Age-reliant increment of hydroxymethylation in the brain cortex in the triple-transgenic mouse design of Alzheimer’s illness. J. Alzheimers Dis. 41, 845–854 (2014).
Trishina, E. et al. Defects in mitochondrial characteristics and metabolomic signatures of developing energetic tension in mouse designs of familial Alzheimer’s illness. PLoS ONE 7, e32737 (2012).
David, D. C. et al. Proteomic and practical analysis reveal a mitochondrial dysfunction in P301L tau transgenic mice. J. Biol. Chem. 280, 23802–23814 (2005).
Ittner, L. M. et al. Parkinsonism and impaired axonal transportation in a mouse design of frontotemporal dementia. Proc. Natl Acad. Sci. U.S.A. 105, 15997–16002 (2008).
Duboff, B., Götz, J. & Feany, M. B. Tau promotes neurodegeneration through DRP1 mislocalization in vivo. Neuron 75, 618–632 (2012).
Cummins, N., Tweedie, A., Zuryn, S., Bertran-Gonzalez, J. & Götz, J. Disease-associated tau hinders mitophagy by hindering parkin translocation to mitochondria. EMBO J. 38, e99360 (2018).
Evans, H. T., Benetatos, J., van Roijen, M., Bodea, L. G. & Götz, J. Decreased synthesis of ribosomal proteins in tauopathy revealed by non-canonical amino acid labelling. EMBO J. 38, e101174 (2019).
Saito, T. & Saido, T. C. Neuroinflammation in mouse designs of Alzheimer’s illness. Clin. Exp. Neuroimmunol. 9, 211–218 (2018).
Reinitz, F. et al. Inhibiting USP16 saves stem cell aging and memory in an Alzheimer’s design. eLife 11, e66037 (2022).
Yu, W. H. et al. Macroautophagy—an unique β-amyloid peptide-generating path triggered in Alzheimer’s illness. J. Cell Biol. 171, 87–98 (2005).
Sun, J. et al. Fecal microbiota hair transplant reduced Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice. Transl. Psychiatry 9, 189 (2019).
Dodiya, H. B. et al. Gut microbiota-driven brain Aβ amyloidosis in mice needs microglia. J. Exp. Med. 219, e20200895 (2022).
Seo, D. O. et al. ApoE isoform- and microbiota-dependent development of neurodegeneration in a mouse design of tauopathy. Science 379, eadd1236 (2023).
Heneka, M. T. et al. NLRP3 is triggered in Alzheimer’s illness and adds to pathology in APP/PS1 mice. Nature 493, 674–678 (2013).
Jiang, S. et al. Proteopathic tau primes and triggers interleukin-1β through myeloid-cell-specific MyD88- and NLRP3–ASC–inflammasome path. Cell Rep. 36, 109720 (2021).
Lafay-Chebassier, C. et al. mTOR/p70S6k signalling modification by Aβ direct exposure along with in APP-PS1 transgenic designs and in clients with Alzheimer’s illness. J. Neurochem. 94, 215–225 (2005).
Caccamo, A., Majumder, S., Richardson, A., Strong, R. & Oddo, S. Molecular interaction in between mammalian target of rapamycin (mTOR), amyloid-β, and tau: impacts on cognitive problems. J. Biol. Chem. 285, 13107–13120 (2010).
Dorigatti, A. O. et al. Brain cellular senescence in mouse designs of Alzheimer’s illness. Geroscience 44, 1157–1168 (2022).
Zhang, P. et al. Senolytic treatment minimizes Aβ-associated oligodendrocyte progenitor cell senescence and cognitive deficits in an Alzheimer’s illness design. Nat. Neurosci. 22, 719–728 (2019).
