Cov Yam Tseem Ceeb Ntawm Alzheimer's Disease Thiab Rheumatoid Arthritis—Pathomechanism Thiab Kev Kho Mob Ntu 3

Nyob rau hauv lem, Kao et al. [106], hauv kev tshawb fawb txog kev tswj hwm ntawm 2271 cov neeg mob nrog AD thiab 6813 cov neeg mob hauv pawg tswj tsis muaj AD, qhia txog kev sib raug zoo ntawm yav dhau los AD thiab RA.

Thaum koj muaj hnub nyoog, koj puas pib xav tias koj lub cim xeeb tau poob qis, lossis feem ntau tsis nco qab tej yam tseem ceeb uas yuav tsum tau ua lossis cov ntaub ntawv muaj xws li npe thiab xov tooj? Qhov tshwm sim no muaj ntau heev hauv lub neej, thiab tib neeg feem ntau ntaus nqi rau nws lub hnub nyoog. Txawm li cas los xij, cov kev tshawb fawb tau pom tias tsis muaj kev sib raug zoo ntawm AD (Alzheimer's disease) thiab nco tsis tau.

Ua ntej ntawm tag nrho cov, peb yuav tsum paub hais tias tsis nco qab yog ib txwm physiological tshwm sim. Thaum peb muaj hnub nyoog, peb lub hlwb pib txo qis thiab kev ua haujlwm ntawm cov neurons maj mam tsis muaj zog, uas ua rau nco tsis tau. Tab sis tsis zoo li AD, ib txwm muaj hnub nyoog txog kev nco tsis tau mus txog qib loj, thiab nws tsuas yog cov txheej txheem qeeb, tsis yog tshwm sim tam sim ntawd.

Qhov thib ob, AD yog ib qho kab mob tsis muaj hnub nyoog uas feem ntau tshwm sim hauv cov hnub nyoog nruab nrab thiab cov neeg laus dua 50 xyoo. Cov neeg feem ntau ntseeg yuam kev tias txhua tus yuav raug kev txom nyem los ntawm AD hauv lawv cov xyoo tom ntej, tab sis qhov no tsis yog li ntawd. Cov neeg laus feem ntau muaj kev nco thiab kev txawj ntse heev, lawv tseem tuaj yeem ua neej nyob zoo, thiab ua lub luag haujlwm tseem ceeb hauv kev sib raug zoo thiab tsev neeg lub neej.

Thaum kawg, kev tswj xyuas lub cev thiab lub hlwb kom zoo yog txoj hauv kev zoo tshaj plaws los tiv thaiv AD thiab nco tsis tau. Ua tib zoo saib xyuas kev hloov pauv hauv lub neej, ua haujlwm ntau lub cev, koom nrog kev xav thiab kev sib raug zoo hauv zej zog yog txoj hauv kev zoo kom lub hlwb noj qab haus huv. Tsis tas li ntawd, koj yuav tsum tswj hwm kev noj qab haus huv thiab kev pw tsaug zog, noj cov zaub mov kom raug, thiab tsis txhob siv tshuaj ntau dhau thiab haus dej kom koj lub cev noj qab haus huv.

Hauv ntej, AD tsis yog ib qho teeb meem uas txhua tus neeg laus yuav ntsib. Txawm tias thaum muaj hnub nyoog laus, kev nco tsis tuaj yeem tiv thaiv thiab tswj tau los ntawm kev noj qab haus huv thiab kev ua neej nyob. Tsuav yog peb tuav tus cwj pwm zoo thiab coj tus cwj pwm zoo, peb muaj peev xwm tuav tau lub hlwb noj qab haus huv thiab nco ntsoov muaj zog. Nws tuaj yeem pom tias peb yuav tsum txhim kho kev nco, thiab Cistanche tuaj yeem txhim kho kev nco zoo vim tias nws tuaj yeem tswj hwm qhov sib npaug ntawm cov neurotransmitters, xws li nce qib ntawm acetylcholine thiab kev loj hlob, uas tseem ceeb heev rau kev nco thiab kev kawm. Tsis tas li ntawd, Cistanche tseem tuaj yeem txhim kho cov ntshav khiav thiab txhawb nqa cov pa oxygen, uas tuaj yeem ua kom lub hlwb tau txais cov khoom noj txaus thiab lub zog, yog li txhim kho lub hlwb tseem ceeb thiab kev ua siab ntev.

Nyem Paub txhawm rau txhim kho kev ua haujlwm nco

Lub hnub nyoog nruab nrab ntawm pawg kawm yog 76.5 ± 7.9 xyoo, thaum lub ntsiab lus ntawm pawg tswj yog 76.5 ± 8.3 xyoo. Tom qab kev txheeb xyuas cov ntaub ntawv, qhov sib txawv tseem ceeb tau txheeb xyuas hauv thaj chaw thaj chaw (p < 0.001), theem ntawm nroog loj (p {{10}}}{{ 20}}02), ntshav siab (p <0.001), ntshav qab zib (p=0.027), hyperlipidemia (p <0.001), stroke (p <0.001), thiab kab mob plawv (p <0.001) ntawm cov mob thiab pab pawg tswj tom qab sib phim cov nox, pab pawg hnub nyoog, thiab xyoo ntawm hnub ntsuas.

Tsis muaj qhov sib txawv tseem ceeb hauv cov nyiaj tau los txhua hli ntawm cov xwm txheej thiab pawg tswj hwm. Txoj kev tshawb no tau pom tias qhov pib ua ntej ntawm RA tau cuam tshuam tsis zoo nrog AD txawm tias nyob hauv cov tib neeg uas muaj kev tsis sib haum xeeb.

Txawm hais tias qhov kev sib raug zoo no, cov kws sau ntawv sau tseg tias txoj kev tshawb no tsis suav nrog ntau yam. Ua ntej, cov ntaub ntawv siv los ntawm cov kws tshawb fawb tsis muaj cov ntaub ntawv hais txog qhov muaj cov cim inflammatory.

Dab tsi ntxiv, cov ntaub ntawv tsis muaj kev sib tham hauv tsev neeg thiab qhia txog kev muaj peev xwm genetic predisposition. Cov kws tshawb fawb tau sau tseg tias cov xwm txheej zoo li no tuaj yeem cuam tshuam rau kev paub txog kev ua haujlwm thiab ua rau cov txiaj ntsig ntawm kev tshawb fawb cuav.

Cov ntaub ntawv tseem tsis muaj ntaub ntawv qhia txog kev kuaj biochemical lossis kev kuaj mob. Tsis tas li ntawd, feem ntau ntawm cov neeg Suav tau raug xaiv los ntawm txoj kev tshawb no, uas tsis tso cai rau kev nthuav dav thiab cuam tshuam rau cov pej xeem [106].

Cov lus xaus zoo sib xws tau mus txog los ntawm Policicchio li al. [107], leej twg txiav txim siab tias RAwas cuam tshuam nrog qis qis ntawm AD. Cov kws tshawb fawb tau pom tias tsis muaj kev sib raug zoo ntawm kev siv NSAIDs thiab AD. Cov kev tshawb fawb meta-kev txheeb xyuas suav nrog cov kev tshawb fawb txog yim-tswj thiab ob txoj kev tshawb fawb pej xeem. Txoj kev sib raug zoo tau txiav txim siab raws li MR tau tham ua ntej.

Kev txheeb xyuas yav dhau los ntawm cov ntawv nyeem tau pom tias RA tau cuam tshuam nrog qhov qis dua ntawm AD. Cov kws sau ntawv ntawm txoj kev tshawb fawb nug qhov kev xav no vim tias MR tsom xam tsis pom muaj kev sib raug zoo ntawm AD thiab RA. Txawm hais tias muaj pov thawj kev kis kabmob los txhawb kev siv tau ntawm qhov kev thov, cov kws sau ntawv lees paub tias tsis muaj kev sib raug zoo ntawm cov kab mob no.

Cov kws tshawb nrhiav pom tias muaj kev cuam tshuam loj rau qhov siv tau ntawm qhov kev tshawb fawb no cuam tshuam los ntawm cov khoom cuam tshuam nrog kev tshawb fawb xws li kev xaiv yuam kev lossis kev kuaj mob sib txawv ntawm RA [107].

Yog li ntawd, cov ntaub ntawv qhia tau hais tias qhov mob yog ib qho ntawm ob qho tib si RA thiab dementia, thiab qhov no tau lees paub los ntawm cov kab mob inflammatory biomarkers pom nyob rau hauv ob yam kab mob (xws li, interleukin -6, interleukin -12, C-reactive protein, cav. 3, endothelin-1, resistin, thiab receptors rau cov khoom kawg ntawm cov qib siab glycation) [108].

Tsis tas li ntawd, los ntawm kev soj ntsuam cov kev sib raug zoo ntawm qhov tshwm sim ntawm AD, kev sib raug zoo tseem ceeb ntawm qhov tshwm sim ntawm AD thiab kev tiv thaiv kev tiv thaiv ntau dhau tau qhia.

Cov kev tshawb fawb no tau qhia txog cov caj ces sib tshooj ntawm AD thiab cov kab mob tiv thaiv kab mob [109]. Txawm hais tias muaj cov cim qhia ntawm qhov mob, qhov kev hais no yuav tsum tau kho nrog kev ceev faj. Tej zaum qhov muaj cov cim ntawm qhov mob tsis qhia qhov ua rau-thiab-tshuaj cuam tshuam kev sib raug zoo ntawm cov kab mob no.

Tej zaum AD andRA yog tswj hwm los ntawm lwm cov txheej txheem ntawm kev tsim cov tshuaj tiv thaiv kab mob, thiab tsuas yog qhov tshwj xeeb uas koom ua ke lawv yog qhov muaj cov cim qhia. Lub ntsiab lus no yuav tsum tau ua haujlwm ntxiv los piav qhia txog cov txheej txheem ua tau ntawm kev tsim cov tshuaj tiv thaiv kab mob hauv AD hauv RA thiab hauv ob qho tib si mob.

4. Lub luag hauj lwm ntawm Ntshav-Brain Barrier nyob rau hauv AD thiab RA

Kev cuam tshuam ntawm cov kab mob hauv lub cev (kab mob, cov kab mob pathological, sepsis) cuam tshuam cov kab mob hauv nruab nrog cev; Txawm li cas los xij, nws yuav tsum tau muab sau tseg tias cov ntshav-hlwb barrier (BBB) ​​dhau los ua qhov nruab nrab ntawm RA thiab AD.

Lub siab ua haujlwm ntawm lub cev tiv thaiv kab mob, nthuav tawm los ntawm kev nce siab ntawm cov neeg kho mob inflammatory, cuam tshuam tsis zoo rau cov qauv thiab permeability ntawm cov teeb meem [110]. Raws li kev tshawb fawb tshawb fawb, barrierpermeability hloov pauv hauv cov neeg mob RA. Barrier dysfunction tseem cuam tshuam nrog cov kab mob neurodegenerative, suav nrog AD [111].

Ntawm cov neeg nruab nrab ntawm lub cev tiv thaiv kab mob, cov kab mob cytokines tsim nyog tau txais kev saib xyuas tshwj xeeb, raws li lawv pom tias muaj peev xwm ua tau yooj yim tshaj BBB [112]. Qhov kev thaiv yog hla nrog kev siv ntau yam qauv, uas yog: los ntawm kev dhau los ntawm cov kab mob periventricular [113], los ntawm stimulating thevagus paj hlwb [114], thiab los ntawm kev khi ncaj qha mus rau lub endothelium, uas ua rau qhib lub kaw ntom nti junctions, nkag mus rau hauv lub paj hlwb. cytokine, thiab nws cov dej num hauv cov ntaub so ntswg hlwb [82].Qhov kev sib raug zoo ntawm RA thiab AD tau kawm hauv nas nrog collagen-inducedarthritis (CIA) [115].

Cov qauv no yog tus cwj pwm los ntawm daim duab kho mob ntawm RA. Ntxiv nrog rau kev tiv thaiv kab mob hauv cov kab mob, kev ncaj ncees ntawm BBB kuj tau kawm los ntawm kev ntsuas qhov qhia ntawm A thauj cov proteins hauv cov hlab ntsha ntawm lub hlwb. Kev tshawb fawb pom tias muaj kev nce hauv astrogliosis, theem ntawm peripheral thiab lub hlwb cytokines, thiab ua kom microglia hauv lub hlwb hauv CIA nas piv rau pawg tswj hwm.

Nws yuav tsum tau hais ntawm no tias astrogliosis tau pom nyob rau lub sijhawm ntawm neuronal degradation tsis teb rau kev raug mob, kis kab mob, lossis muaj kab mob neurodegenerative. Thaum txoj kev tshawb fawb no, kev ntsuas permeability tau ntsuas siv sodium fluorescein, thiab pom tias nws tau nce ntau hauv CIA nas.

Cov kev hloov pauv vascular pom tau cuam tshuam nrog kev nthuav qhia ntawm matrix metalloproteinase thiab txo qis ntawm cov proteins nruj. Occludin yog ib qho protein ntau. Kev nthuav qhia ntau ntxiv ntawm RAGE receptorin lub hippocampus, uas koom nrog kev nkag mus ntawm A los ntawm cov ntshav mus rau lub hlwb, kuj tau pom thaum lub sijhawm kawm.

Txhawm rau pom qhov kev thauj ntawm A ntawm BBB hauv CIA nas, tsiaj txhu tau tswj hwm A 42 intravenously. Nws tau pom tias qhov concentrations ntawm A 42 nyob rau hauv lub cortex thiab tag nrho lub hlwb tau muab piv nrog CIA nas thiab pab pawg tswj.

Txawm li cas los xij, nws tau pom tias hauv hippocampus, A theem ntawm CIArats yog kwv yees li 1.8 npaug siab dua li ntawm kev tswj hwm. Qhov kev sib raug zoo no qhia tias muaj kev nce ntxiv ntawm A los ntawm cov ntshav mus rau hippocampus ntawm CIA nas [115].

Nws kuj tau hais tias cov neeg mob RA yog ib pab pawg uas muaj kev cuam tshuam ntawm homeostasis hauv cov hlab ntsha, lub plawv, thiab cov hlab ntsha hlwb. Cov kev tshawb fawb tau ua nyob rau hauv CIA nas thiab tshawb xyuas endothelial dysfunction induced los ntawm chronicinflammation hauv RA. Qhov kev qhia ntawm cov protein nruj yog txiav txim los ntawm immunoblotting thiab occludin immunofluorescence.

Kev txo qis ntawm cov protein koom nrog hauv kev tsim cov junctions nruj (occludins) tau tshaj tawm. Txoj kev tshawb no xaus lus tias barriintegrity yog impaired nyob rau hauv lub pathophysiology ntawm RA [116].

5. Cov tswv yim kho mob Targeting Aggregates lossis Oligomers, uas yog cov ntawv Amyloid uas txaus ntshai tshaj plaws

Tus nqi ntawm cov protein nrhiav pom amyloidogenic txuas ntxiv mus ntxiv, uas ua rau nyuaj rau kev kuaj mob cov neeg mob los ntawm amyloidosis.

Hauv thawj theem ntawm kev kho mob, nws yuav tsum tau txheeb xyuas cov protein amyloidogenic los ua kom paub tseeb thiab siv cov kev kho mob tsim nyog. Kev kuaj mob kom raug yog raws li kev siv cov kev kuaj mob histochemical [117], kuaj biochemical [118], tshuaj ntsuam caj ces [119,120], thiab kev tshawb fawb txog kev ua haujlwm.

Nyob rau theem tam sim no, txoj hauv kev zoo tshaj plaws rau kev kho mob ntawm cov kab mob amyloidosis yog nres lossis txo cov synthesis ntawm amyloid precursor [121]. Nws tau qhia tias kev cuam tshuam ntawm kev qhia ntawm cov noob sib txuas siv cov tshuaj antisenseoligonucleotides thiab kev cuam tshuam me me RNA tuaj yeem txo qis ntawm amyloidogenic precursor.

Cov kev daws teeb meem zoo li no tau muaj txiaj ntsig zoo hauv daim ntawv ntawm kev txo qis ntawm kev sib txuas ntawm amyloidogenic teeb chains [122]. Txawm hais tias muaj txiaj ntsig zoo, kev siv txoj hauv kev tam sim no hauv kev sim tshuaj ntsib qee qhov teeb meem, suav nrog kev hloov pauv ntawm lub hlwb ntawm kev cuam tshuam RNA [123]. Thawj qhov kev tsim kho tshiab hauv kev kho mob ntawm amyloidosis tau ua tiav los ntawm inhibiting proteases, uas yog lub luag haujlwm rau lub cim ntawm amyloidogenic fragments. Nws tau kwv yees tias lub tswv yim no tseem yuav pom daim ntawv thov hauv kev kho mob Alzheimer's disease.

Qhov no yog vim tias lub hom phiaj kho mob hauv AD yog inhibit - thiab -secretases uas tsim cov amyloidogenic peptide [120]. Tsis tas li ntawd, txoj kev kho mob tshiab tau taw qhia rau qhov tseem ceeb ntawm cov tshuaj lipid-txo qis los ntawm pawg statin, uas tuaj yeem tiv thaiv kev loj hlob ntawm AD los ntawm cov txheej txheem cuam tshuam nrog kev hloov kho ntawm lub peev xwm ntawm kev zais cia kom tshem tawm amyloid precursor [124].

Tsis tas li ntawd, cov tshuaj tiv thaiv kab mob siv rau hauv kev kho mob ntawm AD tuaj yeem cuam tshuam ncaj qha rau kev ua haujlwm zais cia [125]. Kev siv cov secretase inhibitors hauv kev kho mob muaj qee qhov kev txwv. Piv txwv li, ib qho ntawm cov secretase inhibitors, R-flurbiprofen (Flurizan TM), muaj kev txwv rau cov neeg mob uas tsis muaj AD thiab tsis cuam tshuam rau cov neeg mob uas muaj AD [126].

Tsis tas li ntawd, qhov kev txwv tseem ceeb ntawm cov kev kho mob no yog qhov tseeb tias -secretases koom nrog ntau yam kev ua haujlwm ntawm lub cev hauv tib neeg. Yog li, nws yog ib qho enzyme tsis tshwj xeeb rau APP, vim tias nws koom nrog kev tswj hwm ntawm tes kev loj hlob thiab kev hloov pauv ntawm cov protein. Qhov tsis txaus ntseeg no ua rau muaj kev phom sij rau tib neeg [127].

Cov txiaj ntsig tsis zoo no ua rau muaj teeb meem tsis zoo hauv kev ua haujlwm nco, myelination, thiab kev sib koom ua ke ntawm lub cev muaj zog [128]. Qhov kev txwv ntawm kev sivsecretase inhibitors kuj yog BBB vim tias cov hlwb endothelial ntawm qhov teeb meem no txwv tsis pub nthuav dav ntawm cov loj lossis hydrophilic molecules.

Tus secretase inhibitor yuav tsum hla BBB thiab cov kab mob neuronal, vim tias cov txheej txheem ntawm kev hloov kho ntawm APP khiav hauv cov endosomes ntawm neurons hauv lub hlwb. Nws kuj tseem paub tias qhov loj tshaj plaws molecular loj tuaj yeem hla BBB yog kwv yees li 550 DA, yog li hauv kev tsim cov tshuaj tshiab, qhov loj ntawm cov molecule yog qhov tseem ceeb [126].

Nws kuj tseem suav hais tias rau kev kho AD, nws yog qhov tsim nyog los kho cov tib neeg hauv "preclinical" (presymptomatic) theem [129] .Txoj kev tshawb fawb tau coj los ntawm kev kho mob tsis ntev los no nrog kev siv mesenchymal qia hlwb (MSC) [130].

Cov hlwb no raug cais tawm ntawm cov pob txha pob txha, adiposetissue, thiab txoj hlab ntaws [131]. Lawv yog cov pluripotent thiab tuaj yeem hloov mus rau txhua hom cell: osteoblasts, chondrocytes, thiab adipocytes. MSCs nthuav tawm ntau yam kev ua ub no thiab cuam tshuam rau kev ua haujlwm thiab kev ua haujlwm ntawm lub cev tiv thaiv kab mob los ntawm kev hloov kho qhov kev loj hlob ntawm cov neeg nruab nrab tseem ceeb ntawm kev tiv thaiv hauv lub cev thiab tau txais kev tiv thaiv.

Kev txhaj tshuaj ntawm MSC rau hauv lub hlwb hauv AD thiab intra-articular hauv RA yog qhov muaj txiaj ntsig zoo vim tias kev ua xua raug txo qis, cell proliferation yog stimulated, thiab cov cim qhia kev coj tus cwj pwm tau txhim kho [132].

Tam sim no, kev cia siab zoo tau muab tso rau hauv aducanumab, uas nyob rau hauv amyloid PET imaging txwv txoj kev pathology ntawm amyloid thiab ua tau zoo ntawm kev txo qis dementia hauv cov neeg mob inphase III kev sim tshuaj [133]. Yog tias cov kev xav tom ntej tau ua tiav, aducanumab yuav dhau los ua thawj cov tshuaj los hloov kho cov kab mob, yog li lees paub qhov siv tau ntawm theanti-amyloid lub tswv yim [133].

Aducanumab txoj kev kho yog txuam nrog kev phiv tshuaj hu ua Amyloid Related Imaging Abnormalities (ARIA). Thaum lub sij hawm kho, nyob rau hauv ib tug micemodel, los ntshav thiab o ntawm lub paj hlwb tau pom, uas ua rau mob taub hau, tsis meej pem, los yog convulsions.

Kev sib piv, Xiong et al. [134] hauv 2021 tsis tau pom cov kev tsis zoo no tom qab kho nrog cov tshuaj tiv thaiv kab mob tshiab tsom rau APOE. Cov tshuaj tiv thaiv no tau txiav txim siab tias HAE-4.

Hauv cov kev tshawb fawb hauv nas uas kho nrog HAE-4, amyloid plaques raug tshem tawm ntawm lub hlwb thiab cov hlab ntsha yam tsis muaj kev pheej hmoo los ntshav mus rau lub hlwb. Dab tsi ntxiv, cov kws tshawb fawb tau taw qhia tias lub paj hlwb cov hlab ntsha tau pom muaj peev xwm nthuav dav thiab nqaim ntawm qhov xav tau, thiab qhov mob hauv lub hlwb tau txo qis [134].

Ib qho tshuaj tiv thaiv monoclonal tsom rau amyloid kuj yog tus neeg sib tw rau kev kho mob-nws yog BAN240, tsim los ntawm Eisai thiab Biogen [135]. Txawm li cas los xij, nws yog qhov muaj feem ntau tias thaum siv ib leeg, cov neeg ua haujlwm no yuav tsis tuaj yeem txwv lossis kho cov kab mob nyuaj ntawm amyloidosis. Muaj kev cia siab zoo hauv kev siv kev sib xyaw ua ke [135].

6. Cov lus xaus

Cov kab mob hauv lub cev cuam tshuam rau cov tsos ntawm cov kev hloov pauv neurodegenerative.

Qhov zoo sib xws ntawm AD thiab RA pathomechanisms pom nyob rau hauv kev ua haujlwm ntawm lub cev tiv thaiv kab mob, uas, nyob rau hauv kev cuam tshuam ntawm cov khoom tsim nyog, ua rau cov kab mob inflammatory (piv txwv li, interleukin -6, interleukin -12, C-reactive protein, cav 3, endothelin-1, resistin, thiab receptors rau cov khoom kawg ntawm cov qib siab glycation).

Cytokines kho ntau cov txheej txheem hauv lub cev uas cuam tshuam rau qhov nruj ntawm cov ntshav-hlwb teeb meem, nrog rau nws txoj kev ncaj ncees, thiab nruj me ntsis txo cov kev qhia ntawm occluding-forming junctions. Tsis tas li ntawd, AD andRA yog cov teeb meem cuam tshuam nrog cov kab mob ntawm amyloid.

Nyob rau hauv AD, A plaques ua rau muaj kev cuam tshuam ntawm neurons rau excitotoxicity, poob ntawm synaptic protein, thiab cholinergictransmission, thaum nyob rau hauv RA, cytokine-stimulated amyloid pab txhawb kev degradation ntawm cov pob txha-pob txha.

Qhov tshwm sim ntawm AD yog ntau dua hauv cov neeg mob RA ntau dua li cov neeg noj qab haus huv. Lub hav zoov ntawm kev sib txuas ntawm kev sib txuas tau piav qhia los ntawm kev qhia txog kev sib raug zoo ntawm lub paj hlwb, lub cev nqaij daim tawv, thiab lub cev tiv thaiv kab mob nrog rau cov txheej txheem aging ntawm lub cev. Txawm hais tias muaj ntau yam, qhov kev hais no yuav tsum tau kho nrog kev ceev faj.

Lub xub ntiag ntawm cov cim inflammatory yuav tsis qhia txog kev sib raug zoo ntawm cov teeb meem no. Nws yog qhov ua tau tias AD andRA muaj cov txheej txheem sib txawv thiab qhov zoo tib yam uas lawv muaj nyob rau hauv commonis lub xub ntiag ntawm cov cim qhia.

Lub ntsiab lus no yuav tsum tau ua hauj lwm ntxiv kom paub meej txog cov txheej txheem ntawm kev tiv thaiv kab mob hauv ob qho tib si AD hauv RA thiab ob qho tib si kab mob ib txhij.

Tam sim no, kev kho mob ntawm cov kab mob amyloidoses suav nrog kev txwv tsis pub lossis txo cov amyloid precursor synthesis, inter alia, los ntawm kev cuam tshuam cov kev qhia ntawm cov noob caj noob ces siv antisense oligonucleotides thiab cuam tshuam me me RNA.

Kev tsim kho tshiab hauv kev kho mob amyloidosis kuj tau ua tiav los ntawm inhibiting proteases, uas kuj tseem ua tau zoo hauv kev kho AD. Txoj kev kho tshiab siv mesenchymal stemcells thiab monoclonal antibodies tsom amyloid yog qhov tseem ceeb.

Raws li cov kev kho mob no tsis txaus siab thiab muaj ntau yam kev mob tshwm sim, kev tshawb nrhiav cov tswv yim kho mob uas muaj txiaj ntsig zoo dua thiab muaj kev nyab xeeb dua qub tseem txuas ntxiv mus.

Tus Sau Kev Koom Tes: Sau: PT thiab MH, tshuaj xyuas thiab kho: MH thiab JD Txhua tus kws sau ntawv tau nyeem thiab pom zoo rau cov ntawv luam tawm ntawm cov ntawv sau.

Cov Nyiaj Txiag: Cov kev tshawb fawb no tsis tau txais nyiaj txiag sab nraud.

Institutional Review Board Statement: Tsis siv tau.

Cov Lus Qhia Txog Kev Pom Zoo: Tsis siv tau.

Cov Lus Qhia Muaj Cov Ntaub Ntawv: Tsis siv tau.

Kev tsis sib haum xeeb ntawm kev txaus siab: Cov neeg sau ntawv tshaj tawm tsis muaj teeb meem ntawm kev txaus siab.

Cov ntaub ntawv

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