The potential of solanezumab and gantenerumab to prevent Alzheimer’s disease in people with inherited mutations that cause its early onset

Seripa, Davide; Lozupone, Madia; Solfrizzi, Vincenzo; Imbimbo, Bruno P.; Barulli, Maria Rosaria; Tortelli, Rosanna; Capozzo, Rosa; Bisceglia, Paola; Dimitri, Andrea; Stallone, Roberta; Dibello, Vittorio; Quaranta, Nicola; Daniele, Antonio; Bellomo, Antonello; Greco, Antonio; Logroscino, Giancarlo

doi:10.1080/14712598.2018.1389885

Cited by 34 publications

(26 citation statements)

References 87 publications

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“…Panza et al showed the trial design to evaluate whether solanezumab and gantenerumab could prevent AD in its early onset for people with autosomaldominant AD or cognitively healthy subjects at risk of developing sporadic AD [58].…”

Section: Pharmaceutical Neurorestorative Therapymentioning

confidence: 99%

2018 Yearbook of Neurorestoratology

Huang¹,

Sharma

Lin

et al. 2019

Journal of Neurorestoratology

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The Neurorestoratology discipline is getting worldwide attention from the clinicians, basic scientists, students and policy makers alike. Accordingly, this year too, the discipline has made profound advances and great achievements for the benefit of the mankind. In this report, of the 2018 Neurorestoratology Yearbook, salient features of new developments are summarized. This Yearbook consists 3 key themes namely (i) the new findings on pathogenesis of neurological diseases or degeneration; (ii) the new mechanisms of neurorestorative aspects; and (iii) the achievements and progresses made in the clinical field of neurorestorative therapies. The new trend has emerged in clinical studies that are based on greater levels of evidence-based medical practices both in clinical therapies and clinical trials based on standard designs.

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Section: Pharmaceutical Neurorestorative Therapymentioning

confidence: 99%

2018 Yearbook of Neurorestoratology

Huang¹,

Sharma

Lin

et al. 2019

Journal of Neurorestoratology

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“…I ir II fa ziø ty ri muo se ne bu vo ste bë ta sunkiø ne pa gei dau ja mø reið ki niø, kaip, pa vyz dþiui, tai kant ak ty vià imu no te ra pi jà vak ci na. Vi si iki ðiol su AL at lik ti III fa zës di de lës ap im ties kli ni ki niai ty ri mai (EXPEDITION1, EXPEDITION2, EXPEDITION3 ir ExpeditionPRO) ne pa ro dë pra na ðu mo prieð pla ce bo [32]. Ðiuo me tu ðis vais tas ne be ti ria mas AL pa cien tams su nusta ty ta de men ci ja, ta èiau pra dë ti pre ven ci niai ty ri mai [14].…”

Section: Amiloido Beta ðAlinimo Skatinimas Naudojant Pasyvià Ir Aktyunclassified

“…Jo vie na sri tis jun gia si su Ab1-10 ami no rûgð èiø se ka, o ki ta -su Ab16-26 re gio nu [32]. Gan te re nu ma bas ska ti na se ni li niø plokð te liø ar dy mà, ak ty vuo da mas mik ro gli jà ir fa go ci to zae, ta èiau ne si jun gia su plaz mos be ta ami loi du.…”

Section: Amiloido Beta ðAlinimo Skatinimas Naudojant Pasyvià Ir Aktyunclassified

“…Gan te re nu ma bas ska ti na se ni li niø plokð te liø ar dy mà, ak ty vuo da mas mik ro gli jà ir fa go ci to zae, ta èiau ne si jun gia su plaz mos be ta ami loi du. I fa zës ty ri muo se bu vo ge rai tole ruo ja mas, ta èiau da liai pa cien tø ste bë ti pa ki ti mai vaiz diniuo se ty ri muo se (ARIA-E) [31,32]. 2015 m. bu vo su stabdy tas III fa zës kli ni ki nis ty ri mas, nes vais tas ne pa ro dë reikia mo efek to.…”

Section: Amiloido Beta ðAlinimo Skatinimas Naudojant Pasyvià Ir Aktyunclassified

“…2015 m. bu vo su stabdy tas III fa zës kli ni ki nis ty ri mas, nes vais tas ne pa ro dë reikia mo efek to. Ta èiau bu vo ste bë ta ten den ci ja, kad jis bu vo ga li mai nau din gas tiems pa cien tams, ku riø grei èiau siai ma þë jo hi po kam po tû ris ir blo gë jo tes tø re zul ta tai [32]. Ðiuo me tu vyks ta gan te re nu ma bo III fa zës ty ri mai pro dromi nei AL ir leng vai AL gy dy ti [14].…”

Section: Amiloido Beta ðAlinimo Skatinimas Naudojant Pasyvià Ir Aktyunclassified

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In search of Alzheimer’s disease treatment methods: trends of clinical trials

Pakulaitė

Regelskytė

Audronytė

et al. 2018

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Vilniaus universiteto Medicinos fakulteto Klinikinës medicinos instituto Neurologijos ir neurochirurgijos klinika ÁVADASAlz hei me rio li ga (AL) -lë ti në pro gre suo jan ti, ne gráþ ta mø po ky èiø sme ge ny se su ke lian ti li ga [1]. Tai daþ niau sia demen ci jos prie þas tis, su da ran ti 60-70 % vi sø de men ci jø, o jos pa pli ti mas itin di dë ja il gë jant gy ve ni mo truk mei [2,3]. AL su ke lia di de lae eko no mi nae nað tà, taip pat tam pa vis daþ -nes ne mir ties prie þas ti mi [3]. Stu di jø duo me ni mis, mir tingu mas nuo in sul to ir ðir dies li gø ma þë ja, ta èiau AL, kaip mir ties prie þas tis tarp vy res niø nei 75 me tø am þiaus pa cientø, mi n i ma jau ne ðeð to je, o tre èio je vie to je pa gal daþ ná po kar dio vas ku li niø ir ce reb ro vas ku li niø li gø bei vë þio [3,4]. AL gy dy mo kli ni ki niø ty ri mø pra dþia lai ko mi 1980-1990 m., kai pra dë ti nau do ti cho li nes te ra zës in hi bito riai [5]. 1974 m. Drach man ir Le a vitt su sie jo cen tri niø cho li ner gi niø neu ro nø pa þei di mà su at min ties blo gë ji mu ir am þiu mi, o vë les në se stu di jo se Da vis ir Ma lo ney ap ra ðë cho li ner gi nio Mei ner to bran duo lio (angl. nu cleus basalis of Meynert) pa þei di mà pa cien tams, ser gan tiems AL [6,7]. Ma ny ta, kad cho li ner gi nës sis te mos pa þei di mas, ser gant AL, pa na ðus á do pa mi ner gi nës sis te mos pa þei di mà, sergant Par kin so no li ga [8]. Pir mà já cho li nes te ra zës in hi bi toriø tak ri nà leng vai ir vi du ti nio sun ku mo Alz hei me rio ti po de men ci jai gy dy ti 1993 m. áre gist ra vo JAV Mais to ir vaistø ad mi nist ra ci ja (angl. Food and Drug Ad min is tra tion, FDA), ta èiau jis ne be nau do ja mas dël ne pa gei dau ja mø reið ki niø (virð ki na mo jo trak to simp to mø) ir ma þo efek tyvu mo [9,10]. Nuo to lai ko bu vo at lik ta ir ðiuo me tu vyks ta dau gy bë kli ni ki niø ty ri mø, ta èiau tik 3 cho li nes te ra zës inhi bi to riai (do ne pe zi lis, ri vas tig mi nas (jo pe ro ra li në ir trans der ma li në for mos), ga lan ta mi nas) ir glu ta ma ter gi nae sis te mà vei kian tis me man ti nas ty ri muo se pa ro dë pa kan kamà efek ty vu mà bei sau gu mà ir bu vo áre gist ruo ti gy dy ti AL [10]. Ðie vais tai, skir ti simp to mi niam AL gy dy mui, ðiek tiek pa leng vi na li gos kli ni ki nae ið raið kà, ta èiau jø efek ty vumas në ra di de lis, jie ne vei kia li gos prie þas ties ir ne su stabdo li gos pro gre sa vi mo [10,11]. Pas ku ti nis vais tas AL gydy ti -me man ti nas -Eu ro po je bu vo áre gist ruo tas 2002 m., o JAV -2003 m. [10]. Vais tø, skir tø AL gy dy ti, kli ni ki niai ty ri mai vyks ta jau ke lis de ðimt me èius, ta èiau 15 me tø neran da ma nau jø efek ty viø ir sau giø vais tø.Pas ta rà já de ðimt me tá dau giau sia kli ni ki niø ty ri mø at lieka ma su vais tais, po ten cia liai ga lin èiais mo di fi kuo ti AL ei - Adresas: Gy të Pa ku lai të Vil niaus uni ver si te to li go ni nës San ta ros kli ni kos, Neurologijos cen tras San ta rið kiø g. 2, LT-08661 Vil nius El. pa ðtas gyte.pakulaite@gmail.comSan tra...

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Testing the amyloid cascade hypothesis: Prevention trials in autosomal dominant Alzheimer disease

Levin

Vöglein

Quiroz

et al. 2022

Alzheimer's & Dementia

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Objective:The amyloid cascade hypothesis of Alzheimer disease (AD) has been increasingly challenged. Here, we aim to refocus the amyloid cascade hypothesis on its original premise that the accumulation of amyloid beta (Aβ) peptide is the primary and earliest event in AD pathogenesis as based on current evidence, initiating several pathological events and ultimately leading to AD dementia.Background: An ongoing debate about the validity of the amyloid cascade hypothesis for AD has been triggered by clinical trials with investigational disease-modifying drugs targeting Aβ that have not demonstrated consistent clinically meaningful benefits. Updated Hypothesis:It is an open question if monotherapy targeting Aβ pathology could be markedly beneficial at a stage when the brain has been irreversibly damaged by a cascade of pathological changes. Interventions in cognitively unimpaired individuals at risk for dementia, during amyloid-only and pre-amyloid stages, are more appropriate for proving or refuting the amyloid hypothesis. Our updated hypothesis states that anti-Aβ investigational therapies are likely to be most efficacious when initiated in the preclinical (asymptomatic) stages of AD and specifically when the disease is driven primarily by amyloid pathology. Given the young age at symptom onset and the deterministic nature of the mutations, autosomal dominant AD (ADAD) mutation carriers represent the ideal population to evaluate the efficacy of putative disease-modifying Aβ therapies.Major Challenges for the Hypothesis: Key challenges of the amyloid hypothesis include the recognition that disrupted Aβ homeostasis alone is insufficient to produce the AD pathophysiologic process, poor correlation of Aβ with cognitive impairment, and inconclusive data regarding clinical efficacy of therapies targeting Aβ. Challenges of conducting ADAD research include the rarity of the disease and uncertainty of the generalizability of ADAD findings for the far more common "sporadic" late-onset AD. Linkage to Other Major Theories:The amyloid cascade hypothesis, modified here to pertain to the preclinical stage of AD, still needs to be integrated with the development and effects of tauopathy and other co-pathologies, including neuroinflammation, vascular insults, synucleinopathy, and many others.

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The potential of solanezumab and gantenerumab to prevent Alzheimer’s disease in people with inherited mutations that cause its early onset

Cited by 34 publications

References 87 publications

2018 Yearbook of Neurorestoratology

2018 Yearbook of Neurorestoratology

In search of Alzheimer’s disease treatment methods: trends of clinical trials

Testing the amyloid cascade hypothesis: Prevention trials in autosomal dominant Alzheimer disease

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