Nefiracetam hmoovtuaj yeem txhim kho kev txawj ntse thiab tiv thaiv kev puas tsuaj ntawm kev kawm thiab kev nco los ntawm nws cov txiaj ntsig ntawm cerebral cortex. Nws tsis muaj cov yam ntxwv ntawm muscarinic receptor agonists thiab antagonists, los yog inhibit qhov kev ua ntawm acetylcholinesterase. Yog li ntawd, nws tiv thaiv tsis nco qab thiab nco- txhim kho cov nyhuv tshwm sim los ntawm kev txhim kho kev tso tawm ntawm acetylcholine nyob rau hauv lub paj hlwb cortex. Qhov kev ua haujlwm ntawm cov hlab ntsha cholinergic nyob ntawm qhov innervation ntawm cov hlab ntsha glutamatergic, uas tuaj yeem nyob ntawm cov protein kinase ntawm cov chaw pw hav zoov los txhim kho cov haujlwm ntawm Ca2 ntxiv rau channel thiab txhim kho kev tso tawm ntawm acetylcholine. Cov ntaub ntawv tshawb fawb soj ntsuam qhia tiasraw khoom Nefiracetamtej zaum yuav muaj peev xwm los txhim kho kev paub txog kev ua haujlwm thiab kev tiv thaiv neuroprotection. Nyob rau tib lub sijhawm, nws kuj qhia tau tias muaj cov nyhuv antiepileptic.
There is supplementary knowledge about Alzheimer's disease.
In the past two or three decades, the research on Alzheimer's disease (AD) has become more and more in-depth. People continue to improve their understanding of it. The progress of many auxiliary examinations, especially cerebrospinal fluid markers and imaging examination methods, has effectively improved the accuracy of AD diagnosis. In terms of treatment, people also pay more attention to various combined symptoms of AD and strive to improve the quality of life of patients.
On the basis of many studies, many diagnosis and treatment guidelines related to AD have been published at home and abroad, especially the guidelines for the diagnosis and treatment of ad issued by the European Neurology Association in 2010 and the guidelines for the diagnosis and treatment of dementia issued by the Chinese Medical Association in 2010, And the diagnostic criteria for AD (nia-aa criteria) issued by the National Institute on Aging (NIA) and the Alzheimer's Association (AA) in 2011. Based on the above guidelines / diagnostic criteria, we briefly introduce the standardized diagnosis and treatment of AD.
1. txheej txheem kuaj mob AD
1.1 ua kom pom tseeb qhov kev kuaj mob ntawm dementia. Rau cov neeg mob uas muaj kev puas hlwb loj heev, peb yuav tsum xub tsim qhov kev kuaj mob ntawm dementia. Dementia yog ib hom mob syndrome. Thaum cov neeg mob muaj kev txawj ntse lossis kev puas siab puas ntsws thiab ua tau raws li cov yam ntxwv hauv qab no, kev kuaj mob ntawm dementia tuaj yeem txiav txim siab.
(1) Patients' symptoms affect their daily work and life.
(2) Kev paub txog qib thiab kev ua haujlwm tau txo qis piv nrog qhov ua ntej pib.
(3) Delirium thiab lwm yam kab mob puas hlwb (xws li kev nyuaj siab) raug cais tawm.
(4) Raws li keeb kwm kev kho mob thiab lub hom phiaj kev kuaj mob, tus neeg mob tau txiav txim siab tias muaj kev puas siab puas ntsws.
(5) The following cognitive domains and mental symptoms have at least two impairments: ① the ability to learn and remember new information; ② Executive function; ③ Visuospatial ability; ④ Language function; ⑤ There are mental symptoms such as personality and abnormal behavior.
1.2 tom qab tsim qhov kev kuaj mob ntawm AD thiab qhia meej txog kev kuaj mob ntawm dementia, nws yog ib qho tsim nyog yuav tsum tau txiav txim siab ntxiv txog etiology ntawm dementia raws li keeb kwm kho mob, kuaj lub cev, kuaj mob hlwb, kev ntsuam xyuas neuropsychological, kuaj, thiab kuaj xyuas, thiab them nyiaj tshwj xeeb rau kev tsis suav nrog. tej kab mob kho tau.
Cov keeb kwm kev kho mob tam sim no yuav tsum tau them nyiaj mloog rau cov kev paub txog kev puas tsuaj, kev hloov pauv ntawm tus kab mob, cuam tshuam rau kev ua haujlwm niaj hnub thiab lub neej, thiab cuam tshuam txog kev tsis paub meej. Vim tias cov neeg mob dementia muaj kev puas hlwb thiab tsis muaj kev paub txog tus kheej -, cov keeb kwm kho mob yuav tsum tau lees paub lossis ntxiv los ntawm cov neeg sab hauv kom ntau li ntau tau.
Kev kuaj lub cev muaj txiaj ntsig zoo rau kev kuaj mob etiological ntawm dementia. Kev kuaj xyuas lub cev thiab lub paj hlwb yuav tsum tau ua kom ntxaws, uas yuav pab tau kom paub qhov txawv ntawm qhov kev tshaj tawm los ntawm vascular dementia, Lewy lub cev dementia, kev loj hlob supranuclear palsy, thiab lwm yam kab mob ua rau dementia.
Kev ntsuam xyuas neuropsychological tuaj yeem ntsuas qhov tseeb seb cov neeg mob puas muaj kev paub tsis zoo, cov yam ntxwv thiab qhov hnyav ntawm kev paub tsis meej, thiab cov tsos mob ntawm kev puas siab puas ntsws. Nws yog ib qho tseem ceeb rau kev kuaj mob dementia.
Kev kuaj mob hauv chav kuaj (xws li ntshav thiab cerebrospinal kua) thiab kev kuaj pom tuaj yeem pab kom paub meej qhov ua rau dementia. Cerebrospinal fluid test (a) 42. Tau protein, phosphorylated tau protein), structural hlwb magnetic resonance imaging (MRI), fluorodeoxyglucose positron emission computed tomography (FDG-}PET), PETA Imaging, single-photon emission computed tomography (SPECT), thiab lwm yam kev kuaj xyuas thiab kev kuaj pom tau txhim kho qhov tseeb ntawm kev kuaj mob AD.
Nia-aa tus qauv faib cov kev kuaj mob ntawm ad dementia rau hauv qhov tshwm sim AD dementia, qhov tshwm sim AD dementia, thiab qhov tshwm sim lossis qhov tshwm sim AD dementia nrog AD cov cim kab mob. Thawj ob yog siv tau rau yuav luag txhua lub tsev kho mob, thiab qhov thib peb yog siv tau rau cov chaw kho mob uas tau ua tiav kev tshaj tawm - txheeb xyuas biomarker. Tam sim no, nws tsuas yog siv rau kev tshawb fawb tshawb fawb. Tsis tas li ntawd, ad dementia tau lees paub los ntawm pathophysiology kuj tau hais.
1.2.1 probable AD dementia can be diagnosed as probable AD dementia if it meets the following core clinical criteria: (1) it meets the above diagnostic criteria of dementia; (2) The onset of the disease is insidious, and the symptoms gradually appear within a few months to years; (3) The patient's subjective report or informed person's observation to obtain a clear history of cognitive impairment; (4) In medical history and physical examination, the impairment of the initial and most prominent cognitive domain is often memory impairment, in addition, there should be a cognitive domain impairment; (5) When there is evidence of cerebrovascular disease, Lewy body dementia, frontotemporal dementia, and other diseases, ad dementia should not be diagnosed.
1.2.2 qhov ua tau ad dementia muaj ib qho ntawm cov xwm txheej hauv qab no, uas yog, nws raug kuaj pom tias ua tau ad dementia: (1) cov kab mob no tsis raug thiab ua tau raws li Tshooj 1 thiab 4 ntawm cov txheej txheem kho mob saum toj no, tab sis kev txawj ntse. Kev puas tsuaj tuaj yeem tshwm sim tam sim ntawd, lossis keeb kwm kev kho mob tsis ntxaws txaus, lossis cov pov thawj ntawm lub hom phiaj kev paub txog kev poob qis tsis txaus; (2) Lub etiology tsis paub meej thiab ua tau raws li (1) (4) ntawm cov saum toj no- tau hais txog cov txheej txheem kho mob tseem ceeb ntawm AD, tab sis muaj pov thawj ntawm kab mob cerebrovascular, Lewy lub cev dementia, thiab lwm yam kab mob.
1.2.3 ua tau los yog ua tau ad dementia nrog AD pathophysiological cov cim tau qhia txog cov kua cerebrospinal thiab cov cim ntsuas raws li kev kuaj mob saum toj no.
nia-aa tus qauv faib cov biomarkers no ua ob pawg. (1) Brain a Marker of deposition: cerebrospinal fluid a 42 txo thiab pet a Imaging. (2) Biomarkers ntawm neuronal raug mob: nce tau protein nyob rau hauv cerebrospinal kua, txo cov piam thaj metabolism hauv lub cev - parietal cortex los ntawm FDG-PET, atrophy ntawm basal, medial, los yog lateral temporal lobe, thiab atrophy ntawm medial parietal cortex los ntawm cov qauv MRI.
1.2.4 ad dementia tau lees paub los ntawm pathophysiology tuaj yeem kuaj tau raws li ad dementia tau lees paub los ntawm pathophysiology yog tias tus neeg mob ua tau raws li cov txheej txheem kho mob saum toj no thiab kev txawj ntse ntawm ad dementia thiab ua pov thawj muaj nyob ntawm AD pathology los ntawm kev kuaj mob neuropathological.
Kev kho cov tsos mob txawv txav ntawm kev puas siab puas ntsws hauv Ad
EFNS thiab APA cov lus qhia rau tsis yog - tshuaj kho cov tsos mob ntawm kev puas siab puas ntsws (BPSD) qhia nrhiav kev txhawb siab rau BPSD hauv cov neeg mob AD, xws li seb lawv puas muaj kev tsis xis nyob hauv lub neej, ib puag ncig, thiab lub cev, kho lawv lub peev xwm. ua rau, thiab noj kev tswj tsis tau tshuaj (Qib C).
Selective serotonin (5-HT) reuptake inhibitors (SSRIs) es tsis txhob tricyclic antidepressants tuaj yeem ntxiv qhov txo qis ntawm 5-HT los ntawm AD pathology thiab txhim kho kev nyuaj siab ntsig txog neuropsychiatric cov tsos mob, xws li aggression, ntxhov siab vim, apathy, thiab lub hlwb. Cov kab mob tricyclic antidepressants (xws li amitriptyline thiab imipramine) muaj cov tshuaj tiv thaiv kab mob tsis zoo thiab yuav tsum zam.
Antipsychotics tuaj yeem tswj tau BPSD hauv cov neeg mob AD, tab sis lawv cov kev cuam tshuam tsis zoo yog qhov loj thiab yuav tsum tau siv me me ntawm luv luv - lub sij hawm thaum lawv yuav tsum tau siv. Cov kev tsis zoo ntawm cov tshuaj tiv thaiv kab mob atypical xws li aripiprazole, quetiapine, olanzapine, thiab risperidone muaj xws li: ua rau muaj kev pheej hmoo ntawm kev tuag ntawm lub plawv thiab lub paj hlwb, ncua kev tsis sib haum xeeb, qhov hnyav nce, ntshav qab zib, ntau dhau sedation, tsis meej pem, thiab kev paub txog kev ua haujlwm tsis zoo. Yog li ntawd, yuav tsum tau ceev faj txog kev siv cov tshuaj no, cov koob tshuaj qis tshaj plaws yuav tsum tau muab, thiab cov txiaj ntsig thiab kev pheej hmoo ntawm cov tshuaj tiv thaiv kev puas siab puas ntsws rau cov neeg mob thiab lawv tsev neeg yuav tsum raug ceeb toom, tshwj xeeb tshaj yog muaj kev pheej hmoo ntawm kev tuag. Tsis muaj pov thawj tias cov tshuaj tiv thaiv kev puas siab puas ntsws muaj kev nyab xeeb dua li atypical antipsychotics hauv kev pheej hmoo ntawm mob stroke lossis tuag, cov tshuaj siv tshuaj tsis muaj pov thawj tseeb thiab muaj kev phiv ntau dua (Qib B).
Benzodiazepines yuav muaj qee yam cuam tshuam rau cov tsos mob ntxhov siab ntawm cov neeg mob AD. APA cov lus qhia ntseeg hais tias benzodiazepines muaj kev phiv ntau dua thiab muaj txiaj ntsig tsawg dua li cov tshuaj tiv thaiv kab mob. Lawv tsuas yog siv qee zaus hauv cov neeg mob uas muaj qee qhov khaus lossis ntxhov siab, thiab siv sijhawm ntev - yuav tsum zam. Cov kev tsis zoo ntawm benzodiazepines suav nrog kev qaug zog ntau dhau, ua rau muaj kev poob ntau, ua pa nyuaj siab Kev puas hlwb kev ua haujlwm, delirium, thiab muaj kev pheej hmoo ntawm kev nyuaj siab. Lorazepam thiab oxazepam tsis muaj cov tshuaj metabolites, thiab lawv cov teebmeem zoo dua li cov tshuaj uas muaj ib nrab ntev dua - lub neej (diazepam lossis clonazepam), thaum luv luv - cov tshuaj ua yeeb yam muaj ntau dua rau kev poob thiab lub duav pob txha. . Benzodiazepine dependence kuj yog ib qho kev pheej hmoo tsim nyog rau kev mloog.
APA cov lus qhia rau kev siv cov tshuaj stabilizers taw qhia tias kev siv qis - koob tshuaj carbamazepine muaj txiaj ntsig zoo rau cov neeg mob AD provocative tsos mob. Carbamazepine tsis pom zoo ua cov tshuaj siv rau cov neeg mob dementia. Thaum cov tshuaj tiv thaiv kab mob tsis zoo, carbamazepine thiab valproate tuaj yeem txiav txim siab. EFNS cov lus qhia qhia tias carbamazepine yuav pab tau rau tus cwj pwm nruj, tab sis feem ntau valproic acid xeem tsis zoo. Hauv kev xyaum kho mob, tus sau tau pom tias qee cov neeg mob AD muaj cov kab mob ntawm lub cev nqaij daim tawv, uas yog qhov chaw kho mob pom tias yog cov tsos mob ntawm kev puas siab puas ntsws thiab kev coj cwj pwm. Temporal lobe epilepsy yog ib qho yooj yim rau kev kuaj mob tsis zoo raws li cov tsos mob ntawm AD. carbamazepine tuaj yeem tswj cov kev puas siab puas ntsws thiab kev coj tus cwj pwm txawv txav vim los ntawm kev tiv thaiv lub cev lobe epilepsy hauv qee cov neeg mob, thaum nws tuaj yeem tswj tau cov tsos mob ntawm kev puas siab puas ntsws thiab kev coj tus cwj pwm ntawm ad tshwm sim los ntawm nontemporal lobe mob vwm rau lwm tus.
Cov lus qhia rau kev kho mob pw tsaug zog ntseeg hais tias muaj cov ntaub ntawv me me ntawm kev ua tau zoo ntawm nonbenzodiazepines xws li trazodone, zolpidem, lossis zaleplon hauv kev kho mob pw tsaug zog hauv cov neeg mob AD, uas tuaj yeem kho tus kheej nrog rau kev kho mob ntawm cov neeg mob. . Benzodiazepines tsis pom zoo rau kev siv lossis tsuas yog siv sijhawm luv luv - vim tias lawv cov kev cuam tshuam tsis zoo. Diphenhydramine tsis pom zoo vim nws cov nyhuv anticholinergic. Antipsychotics yuav tsum tsis txhob siv tsuas yog los kho kev pw tsaug zog.
Other aids for Alzheimer's disease
Nonsteroidal anti-cov tshuaj tiv thaiv kab mob (NSAIDs) xws li tshuaj aspirin tsis siv rau hauv kev kho mob ntawm AD (theem a) tab sis tuaj yeem siv rau hauv cov neeg mob AD nrog rau lwm cov tshuaj (xws li kev tiv thaiv kab mob plawv). Muaj kev tiv thaiv kab mob pom tseeb- cov tshuaj tiv thaiv kab mob nyob ib puag ncig cov plaques hauv cov neeg mob AD, xws li T lymphocyte infiltration, muaj cov cytokines, ntxiv, thiab tiv thaiv kab mob -txog cov proteins, tab sis qhov tshwm sim no tsis pom nyob rau hauv hnub nyoog- sib phim pawg tswj kev noj qab haus huv. APA cov lus qhia taw qhia tias kev tshawb fawb soj ntsuam ntawm NSAIDs ib leeg, xws li tshuaj aspirin, tsis tau pom tias nws muaj lub hauv paus rau kev kho mob ntawm AD, tab sis cov tshuaj aspirin raug pom zoo thaum tswj cov kev pheej hmoo ntawm AD, xws li kub siab, hyperlipidemia, thiab mob stroke. .
Antioxidants ib leeg tsis muaj lub hauv paus zoo rau kev kho mob ntawm AD, thiab cov lus teb oxidative kev ntxhov siab yog nce Amyloid (a)) Cov teebmeem neurotoxic, antioxidants tuaj yeem tiv thaiv neurons los ntawm Induced neurotoxicity. Piv txwv li, Ginkgo biloba npaj, vitamin E thiab selegiline, cov lus qhia taw qhia tias tsis muaj lub hauv paus los qhia tias kev siv cov tshuaj antioxidants ib leeg tuaj yeem pab cov neeg mob AD. tam sim no, qhov kev tshuaj ntsuam meta- kev soj ntsuam kev nyab xeeb ntawm cov tshuaj vitamin E kuaj pom tias nws muaj kev pheej hmoo ntawm koob tshuaj - nyob ntawm kev tuag. Nws tau pom tias vitamin E yuav tsum tsis txhob siv rau hauv kev kho mob ntawm AD (theem a).
Kev ua tau zoo thiab kev nyab xeeb ntawm kev txawj ntse txhawb cov tshuaj hauv kev kho mob ntawm AD tsis paub meej (qib a). Kev txawj ntse txhawb cov tshuaj muaj xws li lub hlwb metabolic activators (mesylate ergot sib tov, xws li dihydro ergot, nicergoline, thiab lwm yam) thiab pyrrolidone derivatives (piracetam, aniracetam,Nefiracetam, coluracetam). Ergot alkaloids tuaj yeem txhim kho cov metabolism hauv lub hlwb, nce lub luag haujlwm ntawm oxygen uptake thiab qabzib los ntawm lub hlwb hlwb, txhawb cov paj hlwb thiab txhawb kev sib kis ntawm neurotransmitters, txhawm rau txhim kho kev txawj ntse. Pyrrolidone derivatives tuaj yeem ua rau kom lub hlwb metabolic muaj nuj nqi, thiab lawv cov txheej txheem tseem ceeb yog ua rau presynaptic membrane ion channels hauv neurotransmission. Los ntawm kev txhim kho qhov muaj peev xwm tam sim no - nyob ntawm calcium channels ntawm paj hlwb, kev noj cov calcium ions yog txhim kho, thiaj li txhawb kev tso tawm cov neurotransmitters. Cov lus qhia tsis pom zoo kom siv cov tshuaj no niaj hnub, tab sis lawv kuj tau taw qhia tias cov kws kho mob feem ntau siv lawv hauv cov neeg mob xaiv lossis kev kho mob ntxiv vim tias lawv cov txiaj ntsig thiab kev nyab xeeb tsis paub tseeb.
The adjuvant treatment of drugs to improve cerebral blood circulation in AD patients has obvious cerebral vascular amyloidosis (CAA) and cerebral atherosclerosis, which can lead to cerebral vascular stenosis and cerebral ischemia. Positron emission tomography (PET) and single-photon emission computed tomography (SPECT) have verified the phenomenon of reduced cerebral blood flow perfusion in AD patients, although none of the guidelines involves the field of traditional Chinese medicine, However, at present, China's traditional Chinese medicine community is carrying out a lot of research on the treatment of ad with traditional Chinese medicine to improve cerebral blood circulation, which can reduce the damage of nerve cell function caused by secondary cerebral ischemia. The exact results need to be clinically verified.
Patients with mild to moderate AD can use cognitive stimulation or rehabilitation therapy (good practice reference). Professional cognitive rehabilitation therapy can improve patients' function and reduce the need for care (Level B). The guidelines suggest that it should be supplemented by rehabilitation therapy, including (1) stimulation-oriented therapy, such as recreational activities, art therapy, music therapy, and pet therapy. (2) Emotion-oriented therapy, that is, supportive psychotherapy helps alleviate the early loss of function of patients. (3) Recall therapy has research support for improving emotional and behavioral symptoms. (4) Cognitive-oriented therapy, such as ontology positioning, cognitive retraining, and skill training for special cognitive defects, can not benefit patients for a long time.
Kev kho mob daim ntawv thov ntawm Nefiracetam
Nefiracetamtshuaj kho mobyog siv los kho cov kab mob cerebrovascular. Nws tuaj yeem txhim kho kev txawj ntse thiab tiv thaiv kev puas tsuaj ntawm kev kawm thiab kev nco los ntawm nws cov txiaj ntsig ntawm cerebral cortex. Nws tsis muaj cov yam ntxwv ntawm muscarinic receptor agonists thiab antagonists, los yog inhibit qhov kev ua ntawm acetylcholine enzyme. Yog li ntawd, nws tiv thaiv tsis nco qab thiab nco- txhim kho cov nyhuv tshwm sim los ntawm kev txhim kho kev tso tawm ntawm acetylcholine nyob rau hauv lub paj hlwb.