Ukutya kwe-Ketogenic: Indlela engenakulinganiswa yokulwa nesifo se-Alzheimer
Ixesha lokufunda eliqikelelweyo: 30 imizuzu
Inqaku lombhali: NjengoMcebisi weMpilo yeNgqondo oneLayisenisi kunye neminyaka eli-16 yamava abucala, ndichithe iminyaka emithandathu edlulileyo ndiguqula abantu abanesifo sengqondo kunye nokuphazamiseka kwengqondo kwi-ketogenic diet. Kwandithatha ixesha elide ukubhala eli nqaku, yaye andiqinisekanga ukuba kutheni. Ndicinga ukuba, njengomntu onengxaki yokuphazamiseka kwengqondo kwimbali yam yempilo, esi sithuba siziva siseemvakalelo kwaye kunzima ukuba nenjongo ngaso. Andizange ndibe nesifo sika-Alzheimer (enkosi ukulunga), kodwa bendinokuphazamiseka kwengqondo komntu onokukhubazeka kwengqondo. Inqanaba loku-1 isifo se-Alzheimer. Kwakhona, njengomcebisi wezempilo yengqondo, ndihlala nezigulana ezibukele abo babathandayo bemka kubo ngenxa yesi sigulo. Uphando lukude kakhulu kwesi sihloko kunokuba kwakunjalo ngoSeptemba 2021 xa ndandiqala le bhlog. Kangangokuba ndiziva ndinentembelo kwingqinisekiso eyomeleleyo endiyenzileyo ekudalweni kwesihloko esithi “Ukutya kwe-Ketogenic: Indlela Engenakuthelekiswa Nanto Yokulwa Isifo sika-Alzheimer.” Kwaye ngoku, into enzulu emathunjini am indixelela ukuba lixesha. Ndibhala eli nqaku lebhlog ngethemba lokuba umntu (onjengawe) uya kuyifumana kwaye afunde ngendlela enamandla yokucotha ngokuphawulekayo okanye ukumisa ukuqhubeka kwesi sifo kubo okanye kumntu amthandayo.
intshayelelo
Andizukungena kwinto esiyiyo isifo sika-Alzheimer okanye izinga lokuxhaphaka kwaso. Ukuba undwendwela esi sithuba, ulapha ukuze ufunde malunga neendlela ezingcono zonyango, kwaye ixesha lingundoqo. Iinkqubo ze-Neurodeergenerative ezifana ne-dementia ziimeko ezithatha ixesha. Okukhona ulinda ixesha elide ukunyanga oonobangela, kokukhona ukonakala ngakumbi. Nangona kunjalo, kubalulekile ukufumana isiphatho kunyango olusele lukhona kunye neentsilelo zabo. Olu lwazi luya kukuvumela ukuba uthelekise kunye neenzuzo ezinokubakho zokutya kwe-ketogenic kuwe okanye kubathandekayo bakho.
Ukhetho lwangoku lonyango lwe-Alzheimer's akukho nto imfutshane emfiliba. Amayeza avunyiweyo ngoku - ngokuqhelekileyo i-cholinesterase inhibitors kunye ne-NMDA receptor antagonists-ijolise ikakhulu ekulawuleni iimpawu kunokujongana neenkqubo zesifo eziqhuba inkqubo ye-neurodeergenerative.
I-Cholinesterase inhibitors njenge-Donepezil (i-Aricept), i-Rivastigmine (i-Exelon), kunye ne-Galantamine (i-Razadyne). La machiza asebenza ngokunciphisa ukuchithwa kwe-acetylcholine, i-neurotransmitter ebandakanyeka kwimemori kunye nokuqonda, ehlala iphelile kwizigulane ze-Alzheimer. Iziphumo ebezingalindelekanga eziqhelekileyo zinokubandakanya isicaphucaphu, ukuhlanza, kunye norhudo.
Abachasi be-NMDA be-receptor njengeMemantine (Namenda). Eli chiza lisebenza ngokulawula umsebenzi we-glutamate, enye i-neurotransmitter edlala indima kwimemori nokufunda. Ukusebenza ngokugqithisileyo kwe-glutamate kunokubangela umonakalo weselula, apho iMemantine izama ukunceda ukukhusela. Imiphumo enokubakho ibandakanya isiyezi, intloko ebuhlungu, kunye nokudideka.
Ngelixa la mayeza anokubonelela ngesiqabu sexeshana kwezinye iimpawu ezinjengokuphazamiseka kwenkumbulo kunye nokubhideka, zihlala zisiba mfutshane ngokudabukisayo ekumiseni okanye nasekunciphiseni ukuqhubeka kwesifo. Ngaphezu koko, la machiza eza ne-litany yeziphumo ebezingalindelekanga ezinokubakhona, ukusuka kwisicaphucaphu kunye norhudo ukuya ekuphazamisekeni okukhulu kwesingqi sentliziyo.
Kodwa kuthekani ngesithembiso samachiza e-anti-amyloid beta (Aβ)? Ezi zithenjiswe njengonyango, kwaye ukuba sibambe ithutyana elide, eli chiza lommangaliso liza kulungisa isifo sika-Alzheimer. Kunene?
La machiza abeka esichengeni impilo yengqondo yexesha elide. Kutheni ke ukuba sisebenzise le nto kwisifo sika-Alzheimer? Kwaye kutheni izazi zemithambo-luvo zinganikeli imvume eyaneleyo yolwazi kwizigulana malunga nemida kunye nobungozi bokusebenzisa amayeza ukuzama ukunyanga iimpawu ze-Alzheimer's? Kwilinge lethu lokuthomalalisa okwethutyana iimpawu, sinokuthi singaqondanga sinyuse umkhondo wesifo ngokubanzi.
Kula macandelo alandelayo, siza kungena nzulu kwiinkqubo ze-pathological ezisisiseko se-Alzheimer's kwaye siphonononge ukuba ukutya kwe-ketogenic kunokunxibelelana njani nezi ndlela-kwaye kutheni unelungelo elipheleleyo lokwazi malunga nalo njengonyango olunokubakho kuwe okanye kumntu omthandayo. .
Ukujongana ne-Brain Hypometabolism kwi-Alzheimer's: Ukuqinisa i-Ketogenic Diet
Umbindi we-Alzheimer's pathology yinto eyaziwa ngokuba yi-brain hypometabolism. Makhe ndikucacise kakuhle ukuba lithetha ukuthini eli gama.
I-Brain hypometabolism ibhekiselele kwimeko yokunciphisa umsebenzi we-metabolic kwingqondo, ebonakala ngokuncipha kokuthathwa kunye nokusetyenziswa kwe-glucose - umthombo wamandla oyintloko kwiiseli zengqondo. Oku kucotha kwemetabolism kuyintlekele ayikokunqongophala nje kwamandla, nangona oko kuya kuba yingozi ngokwaneleyo. Idala i-cascade yeziphumo eziyingozi eziphazamisa ukusebenza kwe-neuronal kwaye iphazamise unxibelelwano phakathi kweeseli zengqondo.
IiNeurons zixhomekeke kakhulu kumandla; nokuba unqongophalo lwamandla oluncinci lunokuba nefuthe elibonakalayo kubuchule babo bokusebenza. Ngaphandle kokukwazi ukusebenzisa i-glucose yepetroli, baye bangasebenzi kakuhle ekugqithiseni izibonakaliso, kwaye ukukwazi kwabo ukwenza uxhulumaniso olutsha, okubalulekileyo ekufundeni kunye nememori, kuphazamisekile. Ngokuhamba kwexesha, i-hypometabolism eqhubekayo ingakhokelela ekulahlekelweni kwee-neurons kunye nokunciphisa okulandelayo kwivolumu yengqondo (ukunciphisa ingqondo), zombini ezi negalelo ekunciphiseni kwengqondo kunye nokuvela kweempawu ezinxulumene neemeko ezifana ne-Alzheimer's Disease. Ke, i-brain hypometabolism imele eyona nto iphambili kwi-pathogenesis yeengxaki ezahlukeneyo ze-neurodeergenerative.
Mandicace gca xa kunokuthiwa esi sivakalisi sokugqibela asifikanga kuwe.
Lo asingombandela wengxoxo-mpikiswano okanye ukruthakruthwano kuluntu lwenzululwazi. Uphononongo lokucinga ngengqondo luye lwabonisa ngokuqhubekayo ukuncitshiswa kokuthathwa kweglucose kwiindawo ezithile zengqondo ye-Alzheimer. Uphononongo oluninzi oluphononongwe ngoontanga lunxibelelanise lo msebenzi unciphileyo wemetabolism kunye nokuncipha kwengqondo kunye nokulahleka kwenkumbulo ophawu lweSifo se-Alzheimer.
Ayilokhonkco elicingelwayo okanye ulungelelwaniso nje kodwa ngumba omiselwe ngokuqinileyo we-pathology yesifo. Ngenxa yoko, i-hypometabolism yobuchopho ayisiyompembelelo yecala okanye isiphumo se-Alzheimer's; yinxalenye engundoqo inkqubo sifo ngokwayo.
Ukujongana nobu bungqina bungenakuphikiswa, ukujolisa kwi-hypometabolism yobuchopho kuvela njengeyona nto ibalulekileyo, isicwangciso esibalulekileyo ekulweni ne-Alzheimer's Disease. Nangona kunjalo, ngaphandle kwendima yayo ephambili ekuqhubekeni kwesi sifo, i-brain hypometabolism ihlala ingaqwalaselwanga ngamayeza angoku okanye unyango oluqhelekileyo lwe-Alzheimer's Disease.
I-Hypometabolic Brain Structure kwi-AD
Njengoko bekutshiwo ngaphambili, kwi-AD, oku kuphazamiseka kwemetabolism kubonakala ngokukodwa kwimimandla ethile yobuchopho ebalulekileyo kwimemori kunye nemisebenzi yengqondo. Imimandla emibini edla ngokubandakanyeka yiparietal lobe kunye ne-posterior cingulate cortex.
I-parietal lobe, ekufuphi nomva wengqondo, inoxanduva lwemisebenzi eyahlukeneyo, kubandakanya ukuhamba kwendawo, ukuhoywa, kunye nokulungiswa kolwimi. Ukonakala kwayo kunokukhokelela kubunzima ekwenzeni le misebenzi, ibonakale njengokulahleka ngokulula, kunzima ukugcina ingqalelo, okanye ukuba nengxaki yokufunda okanye yokuqonda intetho.
I-posterior cingulate cortex, efumaneka embindini wengqondo, idlala indima ebalulekileyo ekubuyiseni imemori kunye nokulawula ingqiqo. Ukungasebenzi kule ndawo kunokuba negalelo kubunzima bokukhumbula ulwazi kunye nokwenza izigqibo, eziyimpawu zeAD.
Njengoko amandla ale mimandla ekusebenziseni ngokufanelekileyo i-glucose eyancipha, ngokunjalo nokukwazi kwabo ukwenza le misebenzi ebalulekileyo, igalelo elibalulekileyo ekunciphiseni kwengqondo okubonwa kwi-AD.
Kodwa andifuni kukunika umbono wokuba ziindawo nje ezimbalwa zobuchopho eziye zibe yi-hypometabolic kwisifo sika-Alzheimer.
Kwi-Alzheimer's Disease, i-brain hypometabolism ayiphelelanga kwindawo enye, kodwa endaweni yoko, ibonakala ngendlela eqhubekayo, echaphazela imimandla eyahlukeneyo ngokuhamba kwexesha. Nangona kuyinyani ukuba i-parietal lobe kunye ne-posterior cingulate cortex ziphakathi kweyona nto iphambili kwaye ichaphazeleke kakhulu, njengoko isifo siqhubela phambili, ezinye iindawo zengqondo nazo zifumana ukunciphisa ukusetyenziswa kwe-glucose kunye nokusetyenziswa.
Ngokucacileyo, i-lobe yangaphambili, isihlalo semisebenzi yethu yolawulo njengokuthatha izigqibo, ukusombulula iingxaki, kunye nolawulo lweemvakalelo, ekugqibeleni iba yi-hypometabolic kumanqanaba amva esi sifo. Oku kwehla kwemetabolism kwi-lobe yangaphambili kunokukhokelela kutshintsho lokuziphatha, ukugwetywa okungalunganga, kunye nobunzima bokwenza imisebenzi yesiqhelo.
Kodwa ingxaki ye-brain hypometabolism ayipheleli nje apho.
Kwisifo i-Alzheimer's, i-brain hypometabolism isasazeka ngokufihlakeleyo ngaphaya kweendawo ezichaphazelekileyo ekuqaleni, ngokuthe ngcembe igubungele yonke i-cerebral cortex, eyona maleko engaphandle yobuchopho enikwe imisebenzi enodidi oluphezulu. Eyona nto ibaluleke kakhulu yilobe yethutyana, ikhaya lehippocampus-inkumbulo yengqondo. Njengoko umsebenzi wemetabolism uyancipha kule mimandla, iimpawu ezinxulumene ne-Alzheimer's, ezifana nokulahlekelwa yimemori, ziya zibonakala. Ukuxhaphaka kolu kuphazamiseka kwemetabolism kugxininisa ukubaluleka okubalulekileyo kokulwa nalo mba ngokuthe ngqo.
Ngokopapasho oluvela kwiziko leSizwe loLwazi lwe-Biotechnology (NCBI), abaphandi baye baqaphela ukunciphisa ukusetyenziswa kwe-glucose kwimimandla ethile yengqondo, ebonisa i-hypometabolism yobuchopho. Esi siganeko senzeka ubuncinane iminyaka eyi-15 (mhlawumbi i-30) ngaphambi kokubonakaliswa okukhulu ngokwaneleyo kweempawu ezinxulumene nesifo se-Alzheimer. Ngelixa kukho ithuba lokusebenzisa umfanekiso wobuchopho kunye nohlalutyo lwe-spinal fluid ukuvavanya umngcipheko wesifo se-Alzheimer kwiminyaka elishumi okanye ngaphezulu ngaphambi kokubonakaliswa kweempawu, kubandakanya ukukhubazeka okuncinci kwengqondo, ungalindelanga ukuba ugqirha wakho akunike eli nqanaba lovavanyo nangaliphi na ixesha kungekudala. . Okwangoku, icandelo lezonyango alizithathi nzulu iimpawu zakho zokuqonda kwangoko ngokwaneleyo ukuba uzinike.
Ngethamsanqa sinokutya kwe-ketogenic-ngokoqobo unyango lwengqondo ye-metabolic.
Ukwenza imeko ye-ketosis itshintshe umthombo wamandla womzimba ukusuka kwi-glucose ukuya kwi-fatty acids, eyohlulwe ibe yimizimba ye-ketone, njenge-beta-hydroxybutyrate kunye ne-acetoacetate.
Ezimbini kwezi ketones, i-beta-hydroxybutyrate kunye ne-acetoacetate, zisebenza ngendlela ehlekisayo ekudluleni ukungasebenzi kwemetabolism yeglucose ebuchotsheni. Zinokuthatyathwa ngokukhawuleza nangokufanelekileyo ziiseli zengqondo ukuze zifumane amafutha, ngaloo ndlela zivuselela ukunikezelwa kwamandla obuchopho.
Ngaba yonke le mvakalelo iyithiyori? Akukho maxhala. Ndiyakukhuthaza ukuba ubukele le vidiyo yobuchopho ngokoqobo ikhanyisela umva ngamandla emva kokufakwa kwenye yale mizimba yeketone kuphononongo lophando.
Kodwa uxelelwe ukuba ingqondo ifuna iglucose! Kuza kwenzeka ntoni kum okanye kumntu wam endimthandayo ukuba sinqumle i-carbs ephantsi? Ingqondo yakho yenza yonke i-glucose efunwa ngumzimba wakho igluconeogenesis, nto leyo ibonelela ngexabiso nangeshedyuli elungileyo. Enyanisweni, ukutya i-carbohydrates eninzi kunokuba kunceda ukudala ingxaki ye-brain hypometabolism ukuqala.
Xa wena okanye umntu omthandayo ethintela ukutya kwakho kwecarbohydrate ixesha elide elaneleyo, umzimba uya kusebenzisa amanqatha okutya okutyayo kunye namafutha atshisayo emzimbeni ukuvelisa iiketoni. Ukuba umntu ongondlekanga okanye unobunzima obuphantsi, kuthetha nje ukuba sonyusa ukutya kwamafutha ukugcina amandla phezulu kwaye sinciphise amandla okuba nako nakuphi na ukwehla kobunzima.
Kuba sithetha ngemetabolism yobuchopho kunye namandla obuchopho, ndifuna ukuba wazi ukuba ukutya kwe-ketogenic akugcini nje ukuhlangula amandla engqondo ngokubonelela ngolunye umthombo wamafutha. Zikwayimizimba ebonisa iimolekyuli.
Kwaye njengoko oko kusebenza kumandla, kufuneka wazi ukuba bajika iindlela zofuzo ezivumela ukuba i-mitochondria eninzi (izityalo zamandla zeeseli) zenziwe kwaye zivumela iindawo zamandla ezikhoyo (mitochondria) ukuba zisebenze ngokufanelekileyo kwaye zisebenze ngcono. Njengoko unokucinga, oku kunenzuzo eninzi esezantsi kunye nemiphumo yokuphilisa kwingqondo ye-Alzheimer enzima kunye nemveliso yamandla.
Kwaye ukulunga kwam, ngaba esi siphumo esinye sokutya kwe-ketogenic asikwazi ukulungisa i-hypometabolism yobuchopho ibe yinto enjalo? Ngaba esi siphumo esinye besingayi kuba lunyango olungcono lulodwa kuphela kunawo onke amayeza esiwasebenzisayo ngoku njengomgangatho wokhathalelo? Ewe! Ngokuqinisekileyo bekuya kuba njalo. Kwaye bendiya kulishiya eli nqaku ngelo xesha kwaye ndikuthumele kwindlela yakho eya empilweni yakho (okanye eyabo ubathandayo). Kodwa eneneni kukho iziphumo ezongezelelweyo ezibonelela ngokutya kwe-ketogenic eziluncedo ekuthobeni okanye ekumiseni ukuqhubeka kwesifo se-Alzheimer. Ndifuna ubazi bonke.
Qhubeka ufunda.
Uxinzelelo lwe-Oxidative kwi-Alzheimer's Disease: Ukusebenzisa i-Ketogenic Power
Ukuqwalasela ukonakala komsebenzi we-mitochondrial ngumqhubi woxinzelelo lwe-oxidative (OS), akufanele kumangalise ukuba uxinzelelo lwe-oxidative luyinxalenye yento eqhuba inkqubo yesifo kwi-Alzheimer's disease (AD).
Kwabo batsha kule kota, uxinzelelo lwe-oxidative luchaza ukungalingani okwenzeka emizimbeni yethu phakathi kweeathomu ezinobungozi ezibizwa ngokuba yi-oxygen esebenzayo (ROS) kunye nokukwazi kwethu ukukhusela kubo. Awukwazi ukuphila kwaye ungenzi i-ROS, njengoko ziyingxenye eqhelekileyo ye-metabolism, kodwa kwingqondo ye-Alzheimer, uxinzelelo lwe-oxidative luphuma kwiitshathi, kwaye ukungakwazi kwengqondo ukulwa nayo kuqhuba ukuqhubela phambili kwesifo, kubangela umonakalo kwi-neurons yethu. iiprotheni, kunye neDNA. Lo monakalo yinto esiyibhekisela kuyo njengoxinzelelo lwe-oxidative. Kodwa lukhangeleka njani uxinzelelo lwe-oxidative xa lusenzeka engqondweni? Kubonakala ngathi i-lipid peroxidation kunye neprotheyini ephosakeleyo.
Abaqhubi bexinzelelo lwe-Oxidative kwi-Alzheimer's
I-Lipid peroxidation yenye yezona ziphumo eziqhelekileyo zoxinzelelo lwe-oxidative. Iyonakalisa kakhulu ii-neuron ngenxa yokuba i-plasma membranes iqulethe izixa eziphezulu ze-polyunsaturated fatty acids. I-Polyunsaturated fatty acids ichaphazeleka kwi-oxidation. Le nkqubo itshintsha iipropati ze-membrane yeseli, echaphazela ukuguquguquka kwayo, ukunyanzeliswa, kunye nomsebenzi weeprotheni eziboshwe kwi-membrane. Le itanki ibalulekile kwimisebenzi ye-neuronal kunye nokukwazi kwee-neuron ukunxibelelana enye kwenye.
I-protein oxidation ikhokelela ekuguqulweni kwesakhiwo seprotheni kunye nomsebenzi. Oku kunokuphazamisa umsebenzi we-enzyme kunye nomsebenzi we-receptor, ukuvimbela i-neurons yesiqhelo se-biochemical kunye neenkqubo ze-metabolic.
Kwaye sibona ntoni kwingqondo ye-Alzheimer, ukulwa nezixa ezikhulu zoxinzelelo lwe-oxidative?
Uxinzelelo lwe-oxidative lunokwandisa ukuveliswa kwe-amyloid-beta kunye nokuqokelela. Le peptide inokubangela uxinzelelo lwe-oxidative ngokwayo, idale umjikelo okhohlakeleyo womonakalo. Ngaphezu koko, iiprotheyini ezonakaliswe yi-oxidatively kunye ne-lipids ziyakwazi ukwenza i-aggregates, enokuthi ikhulise ukubunjwa kwe-amyloid-beta plaques.
Indima yoxinzelelo lwe-oxidative ibonakala kwi-hyperphosphorylation ye-tau, enye impawu ye-Alzheimer's. Ngaphantsi kweemeko zokuxinzezeleka kwe-oxidative, kukho ukwanda kokusebenza kwe-kinases ezininzi (i-enzymes ezongeza amaqela e-phosphate kwezinye iiprotheni), ezinokukhokelela kwi-tau hyperphosphorylation. I-Hyperphosphorylated tau ixhomekeke ngakumbi ekuhlanganiseni, ekhokelela ekubunjweni kwe-neurofibrillary tangles, enye impawu ye-AD.
Ukongeza, uxinzelelo lwe-oxidative lunokukhokelela ekufeni kwe-neuronal kwi-AD ngenkqubo ebizwa ngokuba yi-apoptosis okanye ukufa kweseli ecwangcisiweyo. Ukubonakaliswa okungapheliyo kuxinzelelo lwe-oxidative kunokubangela le ndlela, ekhokelela ekulahlekelweni kwe-neurons kunye nokunyuka kweempawu zengqondo.
Mandiyithethe loo nto kwakhona, ngenye indlela, ukuba loo nto ayizange ifike ekhaya ngenxa yakho.
Uxinzelelo lwe-oxidative aludlali nje indima yomntu obukeleyo kwisifo sika-Alzheimer. Olu ayilonxibelelwano nje lombutho olufumaneka kuncwadi lwenzululwazi. Uxinzelelo lwe-oxidative kwingqondo ye-Alzheimer's inamandla kwaye ingenangqondo iqhuba ngokusebenzayo ukukhula kunye nokuqhubela phambili kwesi sifo. Ulawulo lwayo olungaqwalaselwanga lubangela kwaye lukhawulezise ukuwohloka kwengqondo, ngokungayekeleliyo kuqhubela phambili ukuwohloka okuphawula isifo sika-Alzheimer.
Uxinzelelo lwe-oxidative olungaqwalaselwanga luqhuba iziganeko ze-neurochemical ezikhokelela ekwakhiweni kweempawu ze-Alzheimer's charactermarks: i-amyloid-beta plaques kunye ne-tau tangles.
Kutheni uxinzelelo lwe-oxidative lungaqwalaselwanga kwingqondo ye-Alzheimer? Kuba amayeza esiwaphuhlisayo esi sifo akabuyeli ngokwaneleyo emva kwikhonkco le-causation ukuze asinike nantoni na esinethemba ngayo. Abawalungisi amandla obuchopho. Abajongani ne-cascade yoxinzelelo lwe-oxidative oluza kwiimeko ezininzi ze-Alzheimer's disease ukusuka kwintlekele yamandla obuchopho.
Ngethamsanqa, sinokutya kwe-ketogenic esinakho ukunceda ukulwa noxinzelelo lwe-oxidative kwingqondo yesifo se-Alzheimer.
Kodwa zeziphi iindlela apho ukutya kwe-ketogenic kufeza oku?
Izidlo ze-Ketogenic zinciphisa uxinzelelo lwe-Oxidative
Okokuqala, ukwandisa amandla engqondo kunye nokuphucula inani le-mitochondrial kunye nomsebenzi oyinxalenye yokutya kwe-ketogenic, uncedo olukhulu ukulwa noxinzelelo lwe-oxidative. IiNeurons zidinga amandla okwenza umsebenzi osisiseko kunye nokugcina iiseli! Ukwazi kangakanani ukwenza imisebenzi yakho yasekhaya okanye umsebenzi xa ungenawo amandla? Akukho kuhle kakhulu? Izinto ziyafumba, kwaye izinto azifezekanga okanye azenziwanga kakuhle? Ngokuchanekileyo. Ingqondo yakho idinga ukuhlangulwa kwamandla okwenzeka kwi-ketogenic yokutya ukuze ugcine uxinzelelo lwe-oxidative kwaye ulawule ukulinganisela phakathi koxinzelelo lwe-oxidative kunye ne-ROS kwingqondo.
I-β-hydroxybutyrate (BHB), umzimba oyintloko we-ketone oveliswa ngexesha le-ketosis, ifunyenwe inezinto ze-antioxidant. Ukunciphisa i-ROS kufezekiswa ngokuphucula ukusebenza kakuhle kwekhonkco lokuthutha i-electron kwi-mitochondria, ukunciphisa ukuvuza kwe-electron kwaye, emva koko ukubunjwa kwe-ROS. Ngokunciphisa imveliso ye-ROS yonke, i-BHB inokunciphisa ngokungathanga ngqo umthwalo woxinzelelo lwe-oxidative.
Kodwa ukutya kwe-ketogenic kunezinye iindlela ezinamandla apho kunceda ukunciphisa uxinzelelo lwe-oxidative. Ukutya kwe-Ketogenic kuboniswe ukuba kukwazi ukunyusa i-endogenous enamandla (eyenziwe emzimbeni wethu) i-antioxidant eyaziwa ngokuba yi-glutathione (GSH).
Ukwanda kwemveliso ye-glutathione esiyibonayo kwi-ketogenic yokutya kunokwenzeka ngenxa yokuba i-ketosis ikhuthaza ukuveliswa kwe-NADPH, i-coenzyme edlala indima ebalulekileyo ekuhlaziyweni kwe-glutathione. Xa iiseli zinokubonelelwa okwaneleyo kwe-NADPH, ziyakwazi ukuguqula ngokufanelekileyo i-glutathione oxidized (GSSG) ibuyele kwifomu yayo encitshisiweyo, esebenzayo (GSH), ngaloo ndlela igcina i-antioxidant yokukhusela.
Ngokuxhasa imveliso kunye nokuhlaziywa kwe-glutathione, i-BHB inceda ukugcina i-pool esebenzayo, iyancipha i-glutathione ekulungele ukumisa i-ROS kunye nokunciphisa uxinzelelo lwe-oxidative ngokubonisa iipropati zayo ezizimeleyo ze-antioxidant. Olu lwalamano lwe-symbiotic phakathi kwe-BHB kunye ne-glutathione lusebenza ukuqinisa ukukhuselwa kwe-antioxidant, kubaluleke kakhulu kwingqondo apho uxinzelelo lwe-oxidative lunokuba nemiphumo emibi.
Kutheni singasebenzisi ukutya kwe-ketogenic njengokhuselo lomgca wokuqala ngokuchasene nokonakala koxinzelelo lwe-oxidative? Kutheni le ingenakuba lunyango olunamandla olukhethwayo, ngakumbi kumxholo weziphumo ezingonelanga ezingonelanga kuqhubekeko lwesifo se-Alzheimer olunikezelwa njengomgangatho wethu wangoku wokhathalelo?
Ngaba ukuhlangulwa kwamandla engqondo ngomnye umthombo wamafutha, ukonyuka kwe-mitochondrial biogenesis, kunye nepropathi ephuculweyo ye-antioxidant yokunciphisa uxinzelelo lwe-oxidative yanele ukutyumba olu nyango lwe-metabolic lwengqondo njengonyango lonyaka lwe-dementia? Bekuya kuba njalo. Kodwa kholwa okanye hayi, kukho iziphumo ezininzi ze-pleiotropic yokutya kwe-ketogenic oya kufuna ukwazi ngayo.
Ukungalingani kwe-Neurotransmitter kwi-Alzheimer's: I-Keto Effect
Amayeza angenelela kuphela kwibhalansi ye-neurotransmitter kunye nenqanaba lomsebenzi, ngokungafihlisiyo, alahlekile ihlathi lemithi. Bajolise kwimveliso yokugqibela yenkqubo ende, ehlayo ngaphandle kokujongana nokungasebenzi kakuhle kwe-mitochondria, i-metabolism, kunye nommiselo woxinzelelo lwe-oxidative obangela ukuqhubela phambili kwe-pathological kwi-Alzheimer's disease. Kodwa unokuba nomdla malunga nokuba ukutya kwe ketogenic kunokunceda njani kwimiba ye-neurotransmitter esiyibona ikhula kwi-Alzheimer's, ke masiqhubeke nokufunda!
Ngoko makhe sibuyele ekuphononongeni ukungabi nantoni kwamayeza agxininise kwiingxaki ze-neurotransmitter ezibonwa kwi-Alzheimer's disease kodwa kwakhona siqhubele phambili ekuqondeni kwethu indlela ukutya kwe-ketogenic kuyindlela ephezulu yokujongana nayo xa sele isenzeka.
Gcina iHandle kwiGlutamate yakho
Khumbula ngokufunda kwakho kwangaphambili kule post ukuba i-NMDA receptor antagonists efana neMemantine (Namenda) iziyobisi ezimiselweyo kwizame zokulawula umsebenzi we-glutamate. Kwenzeka nje ukuba ukutya kwe-ketogenic kunemiphumo enamandla ngaphandle kwemiphumo emibi.
Kutheni singenako ukunyusa ukutya kwe-ketogenic kule njongo kwaye siphephe imiphumo emibi yesiyezi, intloko ebuhlungu, kunye nokudideka okuyingxenye yala mayeza?
Ukutya kwe-Ketogenic Modulate GABA
Ayisiyiyo yonke into malunga nokunciphisa amanqanaba anetyhefu ye-glutamate, nangona kunjalo. Kufuneka kubekho ulungelelwaniso phakathi kwe-glutamate ye-neurotransmitter ye-excitatory kunye ne-inhibitory neurotransmitter i-gamma-aminobutyric acid (GABA). Enye yeempembelelo eziphambili zokutya kwe-ketogenic kwi-chemistry yengqondo ibandakanya (i-GABA), i-neurotransmitter ephambili ye-inhibitory kwingqondo. Uphando lubonise ukuba imizimba ye-ketone inokunyusa imveliso yengqondo ye-GABA. Oku kubalulekile kwisifo sika-Alzheimer kuba umqondiso we-GABAergic uhlala uphazamiseka kwizigulana ze-Alzheimer, kwaye ukuphuculwa kwethoni ye-GABAergic kunokunceda ukubuyisela ibhalansi kuthungelwano lwe-neural oluphazanyiswa sisifo.
Kwakhona, khumbula ukuba kwintshayelelo, sixoxe ngokusetyenziswa kweklasi yamayeza eyaziwa ngokuba yi-Cholinesterase inhibitors. Injongo yala machiza yayikukunciphisa ukuchithwa kwe-acetylcholine, i-neurotransmitter ehlala iphelile kwizigulane ze-Alzheimer.
Kodwa kuthekani ngeAcetylcholine?
I-Acetylcholine yi-neurotransmitter edlala indima ephambili kwimemori nokufunda kwaye iyancipha ngokuphawulekayo kwisifo se-Alzheimer. Nangona ukutya kwe-ketogenic akunyusi ngokuthe ngqo amanqanaba e-acetylcholine, ixhasa impilo yengqondo ngendlela enceda ukugcina umsebenzi we-acetylcholine. Ngokunciphisa uxinzelelo lwe-oxidative kunye nokuxhasa umsebenzi we-mitochondrial, ukutya kwe-ketogenic kukhusela i-cholinergic neurons (i-neurons esebenzisa i-acetylcholine ukuhambisa iimpawu) kumonakalo.
Ke ukwazi ukuba uxinzelelo lwe-oxidative kunye ne-mitochondria eyonakeleyo inokuphazamisa ukukhutshwa kwe-acetylcholine kunye ne-receptors, kuthekani ngathi siphucula ngokubonakalayo umsebenzi we-mitochondrial kunye nokunciphisa uxinzelelo lwe-oxidative ngokusebenzisa iindlela ezinamandla ezifumaneka kukutya kwe-ketogenic? Ndiyakrokrela ukuba sinokubona amanqanaba e-acetylcholine aphuculweyo kwizigulane ze-Alzheimer ngaphandle kwemiphumo eqhelekileyo yesicaphucaphu, ukuhlanza, kunye nohudo.
Ukunciphisa i-Neuroinflammation kwi-Alzheimer's Disease: Impembelelo yoNyango lwe-Ketosis
I-Neuroinflammation yenzeka xa amajoni akho omzimba ezama ukukhusela ingqondo yakho kusulelo, ukwenzakala, okanye ukuqokelelana okungaqhelekanga kweeprotheyini. Xa i-immune response ibangelwa kwingqondo, i-microglia kunye ne-astrocytes zihlasela ngokusebenzayo isoyikiso. Kwaye njengoko behlasela isoyikiso, bakhupha kwaye bakhulule i-cytokines evuthayo. Kwaye njengakumlo wompu, ezinye iimbumbulu zizakubhabha ngendlela engachanekanga, kwaye kuya kwenzeka umonakalo othile.
Ukuba amanqanaba akho oxinzelelo lwe-oxidative alawulwa kakuhle, ingqondo inokwakha kwakhona kwaye ilungiswe kule nkqubo; ukuba akunjalo, ayenzi. Kwaye ngale ndlela, i-neuroinflammation inceda ukuqhuba iinkqubo ze-neurodeergenerative.
Xa i-neuroinflammation iba yinto engapheliyo kwaye ingayekeleli, iya kuyitshintsha ngokwenyani indlela ezi ziphatha ngayo ezi microglia (i-morphology) kwaye zibenze "bavuse" kwaye babe ndlongondlongo kwindlela yabo yokuziphatha malunga nokujongana nohlaselo. Xa ikwimeko esebenza kakhulu, i-microglia iya kuqala ukutya kwaye itshabalalise ii-neuron ezazigula kuphela kwaye zinokusindiswa!
Unokucinga ukuba amajoni omzimba angasebenzi kakuhle, isithintelo segazi-engqondo esaphukileyo (BBB) asikwazi ukukhusela ingqondo, okanye amanqanaba aphezulu oxinzelelo lwe-oxidative ngenxa ye-glucose hypometabolism (amandla obuchopho obuthathaka) okanye ukungoneli kwe-micronutrient kungaqhuba i-cascade engapheliyo ye-neuroinflammation. . Kwaye ngokungathandabuzekiyo, inokuba negalelo ekuphuhliseni nasekuqhubekeni kwezifo ze-neurodeergenerative, kubandakanya nesifo se-Alzheimer.
Ukuba usaziva ubhidekile kancinci malunga nomahluko phakathi kwe-neuroinflammation kunye noxinzelelo lwe-oxidative kunye nendlela ezinxulumene ngayo, unokufumana eli nqaku lingezantsi liluncedo.
Ngaphambi kokuba singene kwiinkqubo apho ukutya kwe-ketogenic kunciphisa i-neuroinflammation, makhe sihlolisise ukuqonda kwethu ukuza kuthi ga ngoku.
I-Ketones inika amandla ubuchopho kwaye ihlangula amandla engqondo. Ukuba ingqondo ilambile amandla, iba noxinzelelo kwaye ibe yimincili. Uxinzelelo lwe-oxidative ludlula eluphahleni, kwaye i-micronutrients iyancipha ukuzama ukugcina izinto zijonge. I-Neurotransmitters iba ngokungalingani (kunye ne-neurotoxic ngokungalingani kwabo; khumbula i-Glutamate?), Kwaye i-neurotransmitter receptors yabo iyaphuka kwaye iphazamise iindlela zonxibelelwano ezifunekayo ukuze zigcinwe kunye nokusebenza. I-Neuroinflammation yenzeka kwaye iveliswa nge-loop impendulo engapheliyo kwaye ifikelela kwimeko engapheliyo engqondweni.
Siphinde safunda ukuba imizimba ye-ketone inokunyusa amandla e-antioxidant yengqondo ngokuthe ngqo nangokungathanga ngqo. Kwaye ukuba bekunjalo, ngaba izibonelelo zokutya kwe-ketogenic zayeka? Ukuba oko "konke" kukutya kwe-ketogenic kunokubonelela ngenkqubo yengqondo ye-neurodeergenerative efana nesifo se-Alzheimer, ngaba oko bekungayi kwanela? Ngaba besingayi kukhululeka kangangokuba kukho into yokunceda zonke ezo ndlela zokugula ziphucuke?
Besiya kwenjenjalo! Kwaye sinjalo! Kodwa ezo akuzona kuphela iindlela apho ukutya kwe-ketogenic kunceda ukulwa neuroinflammation. Esi sithuba seblogi sinokuma apho. Kodwa ngokwenene ndifuna ukuba uqonde ubuninzi beziphumo ze-pleiotropic ukutya kwe-ketogenic kwimpilo yengqondo, ngoko ke ndingayifumana kwiintloko zabantu bonke ukuba asinawo amayeza enza neqhezu loku!
Ukulawula iMicroglia: Ukutya kweKetogenic okuNgabonwayo kwiNeurological Benefit
Njengoko bekutshiwo ngaphambili, iiseli ze-microglial zidlala indima ebalulekileyo kwi-neuroinflammation.
I-Keto: I-Master Regulator ye-Inflammatory Pathways
Zininzi iindlela ezahlukeneyo ekuthi ngazo ukutya kwe-ketogenic kulwe nokudumba, kwaye iziphumo zoko njengomzimba womqondiso wemolekyuli kwiindlela ezahlukeneyo zokukrala ngenene yenye yezona zinto zinomtsalane kuzo zonke!
Iziphumo zokutya kwe-Ketogenic kwi-NLRP3 inflammasome
Okokuqala, i-BHB (enye yaloo mizimba ye-ketone eyenziwe kwi-ketogenic diet) inqanda into ebizwa ngokuba yi-NLRP3 inflammasome. Le yiprotheyini eyinkimbinkimbi edlala indima ebalulekileyo kwimpendulo ye-immune yemvelo kunye nokudumba. Xa ivuliwe yi-microglia kunye nezinye iintlobo zeeseli, ibangela ukukhululwa kwe-cytokines e-pro-inflammatory efana ne-IL-1β kunye ne-IL-18, enegalelo kwiinkqubo zokuvuvukala emzimbeni.
Izidlo ze-Ketogenic zidlala indima ekuvimbeleni le nkqubo. Ngokuthintela i-NLRP3 inflammasome, i-BHB inceda ukunciphisa ukukhululwa kwe-cytokines e-pro-inflammatory kunye nokunciphisa impendulo yokuvuvukala.
I-BHB inokuthintela i-NLRP3 inflammasome ngeendlela ezininzi. Ivimbela ukuhlanganiswa kwe-NLRP3 inflammasome complex, ukukhusela ukusebenza kwayo. Ivimbela ukuveliswa kwe-cytokines e-pro-inflammatory efana ne-IL-1β ngokunciphisa ukusebenza kwe-inflammasome. Kwaye inokulungelelanisa umsebenzi we-transcription factor NF-κB, olawula ukubonakaliswa kwezakhi zofuzo ezibandakanyekayo ekudumbeni.
Masifunde eso sivakalisi sokugqibela kwakhona. Ilawula ukubonakaliswa kofuzo olubandakanyekayo ekudumbeni. Ndibonise iyeza le-pharma le-Alzheimer's eyenza oko ngempumelelo.
Izitshixo ze-Ketogenic kwi-HCA2
Enye indima edlalwa yi-beta-hydroxybutyrate (BHB), i-ketone eveliswa kwi-ketogenic diet, intsebenziswano yayo kunye ne-receptor ebizwa ngokuba yi-Hydroxycarboxylic Acid Receptor 2 (HCA2) okanye i-G-protein edibeneyo ye-receptor 109A (GPR109A). Lo mzimba we-ketone ubophelela kwaye usebenze i-HCA2 kunye ithumela umqondiso ngaphakathi kwiseli ukunciphisa ukuvuvukala.
Ngoku makhe sithethe ngeprostaglandins. Iiprostaglandins ziikhemikhali emizimbeni yethu ezidlala indima ekudumbeni. Benza njengabathunywa abahambisa imiqondiso kwiiseli, bebaxelela ukuba bavuthe. I-BHB inciphisa ukuveliswa kwezi prostaglandins. Xa i-BHB isebenze i-HCA2, ithumela isibonakaliso kwiiseli ukuba ziyeke ukuthumela loo miyalezo yombhalo evuthayo. Ngamanye amazwi, i-BHB isebenza njengeqhosha "lokuthulisa" kwiiseli, libathintele ekukhupheni imiyalezo emininzi ekhuthaza ukuvuvukala.
Ngokunciphisa ukuveliswa kweprostaglandin kunye nokunciphisa impendulo yokuvuvukala, i-BHB inceda ukulawula ukuvuvukala emzimbeni. Le yindlela enye yokutya kwe-ketogenic, kunye nokuveliswa kwayo okwandisiweyo kweBHB, kunokuba nemiphumo yokuchasana nokuvuvukala.
Ukutya kwe-Ketogenic: I-Gut-Brain Axis Transformer yokuNqanda ukuvuvukala
I-gut microbiome kucingelwa ukuba inefuthe ekuqhubekeni kwesifo sika-Alzheimer. Kucingelwa ukuba yenze oku nge-microbiome yemveliso ye-metabolites, iimpembelelo kwi-neurotransmitters, ukuguqulwa kwe-immune system kunye nokuvuvukala, kunye nemiphumo enokubakho kwingqibelelo yesithintelo segazi-ingqondo (BBB).
Ukutya kwe-ketogenic kukhokelela kutshintsho olubalulekileyo kwi-gut microbiome. Ikhuthaza ukukhula kwebhaktheriya enenzuzo ngelixa inciphisa ubuninzi beentsholongwane ezinokuba yingozi. Olu tshintsho kulwakhiwo lwe-microbial lubonwa luchaphazela ukusebenza kwengqondo kunye nokudumba nge-axis ye-gut-brain kakhulu.
Ngoba? Ngenxa yokuba i-microbiome ye-gut ivelisa i-metabolites eyahlukeneyo kunye neemolekyuli zokubonisa ezinokusebenzisana nenkqubo ye-nervous. Ezi molekyuli zinokuchaphazela ngokuthe ngqo ukusebenza kwengqondo kunye nokulungelelanisa iinkqubo zokuvuvukala. Amandla okutya kwe-ketogenic okunciphisa ukudumba kunokungenelela, ubuncinci ngokuyinxalenye, ngempembelelo yayo kwi-gut microbiota. Yenye nje indlela yokutya okune-ketogenic kunceda ukulwa neuroinflammation kwaye imodareyitha inkqubo enye yesifo ebonwa kwi-Alzheimer's dementia.
Kutheni le nto singasebenzisi ungenelelo olukhuthaza ukudumba okunempilo ebuchotsheni kumntu ophethwe yinkqubo ye-neurodeergenerative efana nesifo sika-Alzheimer?
Ukuba ufuna ukuqonda imiphumo yokutya kwe-ketogenic kwezinye izinto ezinxulumene ne-microbiome exutyushwa kweli candelo, nceda ubone la manqaku ongezelelweyo angezantsi ngaphambi kokuba uqhubekele kwisigqibo.
Ukuqukumbela: Isifo se-Alzheimer kunye nendima eNgafunekanga ye-Ketogenic Diet
Ke ngaba ukutya kwe-ketogenic kuya kulungisa zonke iindlela ezisisiseko ze-pathological eziyinxalenye yabathandekayo bakho (okanye bakho) ukuhla kwengqondo? Mhlawumbi. Kodwa mhlawumbi akunjalo. Ukuba uxinzelelo lwe-oxidative luqhutywa ngakumbi ngumthwalo wentsimbi enzima, ukuvezwa kwityhefu yokungunda, usulelo olufihlakeleyo, okanye ezinye izinto ezahlukeneyo, uya kufuna okanye ufune uncedo olongezelelweyo. Ukuqhubela phambili kwesifo kunokuqhutywa ngamanqanaba angonelanga okanye anqongopheleyo kwi-micronutrients ebalulekileyo ekufuneka i-mitochondria iphumelele.
Kukho izinto ezahlukeneyo zokuqhuba isifo se-Alzheimer kunye neephenotypes ezahlukeneyo. Injongo yale nqaku ayikukuphikisana okanye ukuxubusha ukuba ngaba ukutya kwe-ketogenic kuya kulungisa zonke iindlela ezisisiseko ze-pathological eziyingxenye yokuqhubela phambili kwesifo esithile.
Inqaku kunye nenjongo yeli nqaku kukukubonisa ukuba ukutya kwe-ketogenic yeyona ndlela yonyango olubanzi kunye ne-neuroprotective esinalo. Ukunxibelelana nawe ngokukuko ukuba kukho nantoni na enethuba lokumisa okanye ukucothisa ukuqhubeka kwesifo i-Alzheimer ngokusebenzisa iindlela ezininzi ezongezelelweyo, oko kukuthi, ngokuphandle, kukutya kwe-ketogenic.
Kwaye okokugqibela, eli nqaku labhalelwa ngethemba ukutshabalalisa imbono engalunganga yokuba unyango olumiselwe ngugqirha wakho wemithambo-luvo lumele iindlela ekukuphela kwazo zokujongana noko bekubonakaliswe ngokungachanekanga njengoqikelelo olubi nolungenakuguqulwa. Andiqinisekanga ukuba kunjalo xa ezi zinto zisisiseko ezichazwe kule post zinikwa ukufikelela kungenelelo olunamandla njengokutya kwe-ketogenic. Ubuncinci, kwiimeko ezininzi, ndicinga ukuba ukucotha kokuqhubela phambili kunokwenzeka.
Sukuhlala phantsi ungenzi nto, ulindele iingcali zezempilo ukuba zifikelele kwisantya sokufunyanwa kwezenzululwazi ngelixa ingqondo yakho okanye umntu omthandayo eqhubeka ne-neurodegenerate ukuya kwinqanaba lokungabuyi.
Unokusebenzisana ne-ketogenic-trained dietician okanye i-nutrist ukubanceda (okanye wena). Ukuba une-Mild Cognitive Impairment (MCI) okanye i-Alzheimer's yenqanaba lamva kwaye unenkxaso yomkhathaleli, unokufumana inkxaso kunye nenzuzo inkqubo yam ye-intanethi.
Nokuba uthatha isigqibo sokuya phi ufuna uncedo, musa ukulinda.
Ndilapha ukukuxelela ukuba akukho mntu uza kukuhlangula okanye umntu omthandayo kwimihlathi yesifo sengqondo esiyingozi. Isenzo sokuphumeza ukutya kwe-ketogenic siyenzeka, kwaye kukho inkxaso eninzi phaya.
Ndikuthumelela uthando kuhambo lwakho.
Ukuba ukhangela ulwazi malunga nee-ketones zangaphandle ungafumana amanqaku alandelayo eluncedo.
Ucaphulo
Achanta, LB, & Rae, CD (2017). I-β-Hydroxybutyrate kwiBrain: I-Molekyuli enye, iiMechanism ezininzi. Uphando lwe-Neurochemical, 42(1), 35-49. https://doi.org/10.1007/s11064-016-2099-2
Almulla, AF, Supasitthumrong, T., Amrapala, A., Tunvirachaisakul, C., Jaleel, A.-KKA, Oxenkrug, G., Al-Hakeim, HK, & Maes, M. (2022). I-Tryptophan Catabolite okanye i-Kynurenine Pathway kwi-Alzheimer's Disease: Ukuphononongwa okuCwangcisiweyo kunye nohlalutyo lweMeta. Ingxelo yeZifo ze-Alzheimer's, 88(4), 1325-1339. https://doi.org/10.3233/JAD-220295
Altayyar, M., Nasser, JA, Thomopoulos, D., & Bruneau, M. (2022). Impembelelo ye-Physiological Ketosis kwi-Cognitive Brain: Uphononongo oluBalisayo. Amanzi, 14(3), iSiqendu 3. https://doi.org/10.3390/nu14030513
Alves, F., Kalinowski, P., & Ayton, S. (2023). Ukulahleka koMqulu weBrain okukhawulezayo obangelwa yi-Anti-β-Amyloid Drugs: Ukuphononongwa ngokuchanekileyo kunye nohlalutyo lweMeta. Neurology, 100(20), e2114-e2124. https://doi.org/10.1212/WNL.0000000000207156
Iimpawu ze-Alzheimer: Iinguqu zengqondo. (nd). Ifunyenwe ngoMeyi 21, 2023, ukusuka https://www.healthline.com/health-news/can-alzheimers-be-detected-30-years-before-it-appears
Ardanaz, CG, Ramírez, MJ, & Solas, M. (2022). Utshintsho lweMetabolic yeBrain kwi-Alzheimer's Disease. I-International Journal ye-Molecular Sciences, 23(7), iSiqendu 7. https://doi.org/10.3390/ijms23073785
Bohnen, JLB, Albin, RL, & Bohnen, NI (2023). Ungenelelo lwe-Ketogenic ekuphazamisekeni kwengqondo encinci, isifo se-Alzheimer, kunye nesifo sika-Parkinson: Uphononongo olucwangcisiweyo kunye novavanyo olubalulekileyo. Frontiers kwi-Neurology, 14, 1123290. https://doi.org/10.3389/fneur.2023.1123290
Costantini, LC, Barr, LJ, Vogel, JL, & Henderson, ST (2008). I-Hypometabolism njengenjongo yonyango kwi-Alzheimer's disease. I-BMC Neuroscience, 9(Ubonelelo 2), S16. https://doi.org/10.1186/1471-2202-9-S2-S16
Croteau, E., Castellano, CA, Fortier, M., Bocti, C., Fulop, T., Paquet, N., & Cunnane, SC (2018). Uthelekiso olunqamlezileyo lwe-glucose yengqondo kunye ne-ketone metabolism kubantu abadala abanempilo enempilo, ukukhubazeka okuphakathi kwengqondo kunye nesifo se-Alzheimer sokuqala. Iingcali zeGerontology, 107, 18-26. https://doi.org/10.1016/j.exger.2017.07.004
Cullingford, TE (2004). Ukutya kwe ketogenic; i-acids enamafutha, i-acid-activated receptors kunye ne-neurological disorders. Prostaglandins, Leukotrienes kunye ne-Essential Fatty Acids, 70(3), 253-264. https://doi.org/10.1016/j.plefa.2003.09.008
Cunnane, S., Nugent, S., Roy, M., Courchesne-Loyer, A., Croteau, E., Tremblay, S., Castellano, A., Pifferi, F., Bocti, C., Paquet, N ., Begdouri, H., Bentourkia, M., Turcotte, E., Allard, M., Barberger-Gateau, P., Fulop, T., & Rapoport, S. (2011). I-METABOLISM YEZIFUTHA ZOBUCHOPHO, UKUGUGA KUNYE NESIFO SE-ALZHEIMER. Isondlo (eBurbank, eLos Angeles County, Calif.), 27(1), 3-20. https://doi.org/10.1016/j.nut.2010.07.021
Dilliraj, LN, Schiuma, G., Lara, D., Strazzabosco, G., Clement, J., Giovannini, P., Trapella, C., Narducci, M., & Rizzo, R. (2022). I-Evolution ye-Ketosis: Impembelelo enokubakho kwiiMeko zeKlinikhi. Amanzi, 14(17), iSiqendu 17. https://doi.org/10.3390/nu14173613
Gano, LB, Patel, M., & Rho, JM (2014). Ukutya kwe-Ketogenic, i-mitochondria, kunye nezifo ze-neurological. Umbhalo wePopid Research, 55(11), 2211-2228. https://doi.org/10.1194/jlr.R048975
Gómora-García, JC, Montiel, T., Hüttenrauch, M., Salcido-Gómez, A., García-Velázquez, L., Ramiro-Cortés, Y., Gomora, JC, Castro-Obregón, S., & Massieu , L. (2023). Umphumo we-Ketone Body, i-D-β-Hydroxybutyrate, kwi-Sirtuin2-Mediated Regulation yoLawulo lweMitochondrial Quality kunye ne-Autophagy-Lysosomal Pathway. Iiseli, 12(3), iSiqendu 3. https://doi.org/10.3390/cells12030486
Grammatikopoulou, MG, Goulis, DG, Gkiouras, K., Theodoridis, X., Gkouskou, KK, Evangeliou, A., Dardiotis, E., & Bogdanos, DP (2020). Ukuya eKeto okanye hayi eKeto? Ukuphononongwa okuCwangcisiweyo kweeMvavanyo eziLawulwayo eziRandomized Ukuvavanya imiphumo ye-Ketogenic Therapy kwi-Alzheimer's Disease. Inkqubela phambili kwiZondlo, 11(6), 1583-1602. https://doi.org/10.1093/advances/nmaa073
Jarrett, SG, Milder, JB, Liang, L.-P., & Patel, M. (2008). Ukutya kwe-ketogenic kwandisa amanqanaba e-mitochondrial glutathione. Journal of Neurochemistry, 106(3), 1044-1051. https://doi.org/10.1111/j.1471-4159.2008.05460.x
Jiang, Z., Yin, X., Wang, M., Chen, T., Wang, Y., Gao, Z., & Wang, Z. (2022). Imiphumo ye-Ketogenic Diet kwi-Neuroinflammation kwi-Neurodeergenerative Diseases. Ukuguga kunye neZifo, 13(4), 1146. https://doi.org/10.14336/AD.2021.1217
Kalani, K., Chaturvedi, P., Chaturvedi, P., Kumar Verma, V., Lal, N., Awasthi, SK, & Kalani, A. (2023). Iindlela zeMitochondrial kwisifo se-Alzheimer: Ukufuna unyango. Ukufunyanwa Kweziyobisi Namhlanje, 28(5), 103547. https://doi.org/10.1016/j.drudis.2023.103547
Kashiwaya, Y., Takeshima, T., Mori, N., Nakashima, K., Clarke, K., & Veech, RL (2000). I-D-β-Hydroxybutyrate ikhusela i-neurons kwiimodeli ze-Alzheimer kunye nesifo sika-Parkinson. Iinkqubo ze-National Academy of Sciences, 97(10), 5440-5444. https://doi.org/10.1073/pnas.97.10.5440
Ukutya kwe-Ketogenic kuphucula ukuphazamiseka kwengqondo kunye neuroinflammation kwimodeli yempuku ye-Alzheimer's disease-Xu-2022-CNS Neuroscience & Therapeutics-Wiley Online Library. (nd). Ifunyenwe ngoMeyi 24, 2023, ukusuka https://onlinelibrary.wiley.com/doi/10.1111/cns.13779
Koh, S., Dupuis, N., & Auvin, S. (2020). Ukutya kwe-Ketogenic kunye ne-Neuroinflammation. Uphando lweSithuthwane, 167, 106454. https://doi.org/10.1016/j.eplepsyres.2020.106454
Kong, G., Wang, J., Li, R., Huang, Z., & Wang, L. (2022). Ukutya kwe-Ketogenic kuphucula ukuvuvukala ngokuvimbela i-NLRP3 inflammasome kwi-osteoarthritis. Uphando lweArthritis kunye nonyango, 24, 113. https://doi.org/10.1186/s13075-022-02802-0
Kumar, A., Sharma, M., Su, Y., Singh, S., Hsu, F.-C., Neth, BJ, Bhalisa, TC, Blennow, K., Zetterberg, H., Craft, S. , & Nzulu, G. (2022). Ii-vesicles ezincinci ze-extracellular kwiplasma zityhila iziphumo zemolekyuli yokutya okuguquliweyo kweMeditera-ketogenic kubathathi-nxaxheba abanokuphazamiseka okuncinci kwengqondo. Unxibelelwano ngengqondo, 4(6), fcac262. https://doi.org/10.1093/braincomms/fcac262
Lilamand, M., Mouton-Liger, F., & Paquet, C. (2021). Unyango lokutya kwe-Ketogenic kwisifo se-Alzheimer: Uphononongo oluhlaziyiweyo. Uluvo lwangoku kwiZondlo zeKlinikhi kunye noNyango lweMetabolic, Papasha Phambi Koshicilelo. https://doi.org/10.1097/MCO.0000000000000759
Macdonald, R., Barnes, K., Hastings, C., & Mortiboys, H. (2018). Ukungahambi kakuhle kweMitochondrial kwisifo sikaParkinson kunye nesifo se-Alzheimer: Ngaba i-mitochondria inokujoliswa ngonyango? I-Biochemical Society Transactions, 46(4), 891-909. https://doi.org/10.1042/BST20170501
Mentzelou, M.; Dakanalis, A.; Vasios, GK; Gialeli, M.; Papadopoulou, SK; Giaginis, C. Ubudlelwane bokutya kwe-Ketogenic kunye ne-Neurodeergenerative and Psychiatric Diseases: Uphononongo lwe-Scoping ukusuka kuPhando oluSiseko ukuya kwi-Clinical Practice. Amanzi 2023, 15, 2270. https://doi.org/10.3390/nu15102270
Milder, J., & Patel, M. (2012). Ukuguqulwa koxinzelelo lwe-oxidative kunye nomsebenzi we-mitochondrial ngokutya kwe-ketogenic. Uphando lweSithuthwane, 100(3), 295-303. https://doi.org/10.1016/j.eplepsyres.2011.09.021
Ukungasebenzi kakuhle kweMitochondrial kwi-pathologies yabantu | DIGITAL.CSIC. (nd). Ifunyenwe ngoMeyi 24, 2023, ukusuka https://digital.csic.es/handle/10261/152309
Murakami, M., & Tognini, P. (2022). IiNdlela zeMolekyuli eziPhantsi kweePropati ze-Bioactive ze-Ketogenic Diet. Amanzi, 14(4), iSiqendu 4. https://doi.org/10.3390/nu14040782
Napolitano, A., Longo, D., Lucignani, M., Pasquini, L., Rossi-Espagnet, MC, Lucignani, G., Maiorana, A., Elia, D., De Liso, P., Dionisi-Vici , C., & Cusmai, R. (2020). I-Ketogenic Diet Yonyuka kwi-Vivo Glutathione Levels kwizigulane ezine-Epilepsy. Metabolites, 10(12), iSiqendu 12. https://doi.org/10.3390/metabo10120504
Pflanz, NC, Daszkowski, AW, James, KA, & Mihic, SJ (2019). Ukumodareyitha komzimba we-Ketone we-ligand-gated ion channels. Neuropharmacology, 148, 21-30. https://doi.org/10.1016/j.neuropharm.2018.12.013
Pietrzak, D., Kasperek, K., Rękawek, P., & Piątkowska-Chmiel, I. (2022a). Indima yoNyango ye-Ketogenic Diet kwi-Neurological Disorders. Amanzi, 14(9), iSiqendu 9. https://doi.org/10.3390/nu14091952
Pietrzak, D., Kasperek, K., Rękawek, P., & Piątkowska-Chmiel, I. (2022b). Indima yoNyango ye-Ketogenic Diet kwi-Neurological Disorders. Amanzi, 14(9), 1952. https://doi.org/10.3390/nu14091952
Raulin, A.-C., Doss, SV, Trottier, ZA, Ikezu, TC, Bu, G., & Liu, C.-C. (2022). I-ApoE kwisifo se-Alzheimer: I-Pathophysiology kunye nezicwangciso zonyango. I-Molecular Neurodegeneration, 17(1), 72. https://doi.org/10.1186/s13024-022-00574-4
Rho, J., & Stafstrom, C. (2012). Ukutya kwe-Ketogenic njengeParadigm yoNyango kwiiDidiversity Neurological Disorders. Imida kwi-Pharmacology, 3. https://www.frontiersin.org/articles/10.3389/fphar.2012.00059
Ribarič, S. (2023). Ukufumanisa ukuNqatshwa kweNgcaciso kwangethuba kwi-Alzheimer's Disease kunye ne-Brain Synaptic Structural and Functional Evaluation. Iintsholongwane, 11(2), iSiqendu 2. https://doi.org/10.3390/biomedicines11020355
Schain, M., & Kreisl, WC (2017). I-Neuroinflammation kwi-Neurodegenerative Disorders-Uphononongo. I-Neurology yangoku kunye neeNgxelo zeNeuroscience, 17(3), 25. https://doi.org/10.1007/s11910-017-0733-2
Sharma, C., & Kim, SR (2021). Ukudibanisa uxinzelelo lwe-Oxidative kunye neProteinopathy kwi-Alzheimer's Disease. Antioxidants, 10(8), iSiqendu 8. https://doi.org/10.3390/antiox10081231
Şimşek, H., & Uçar, A. (2022). Ngaba i-Ketogenic Diet Therapy iSilungiso se-Alzheimer's Disease okanye i-Mild Cognitive Impairments? Ukuqhubela phambili kwiGerontology, 12(2), 200-208. https://doi.org/10.1134/S2079057022020175
Simunkova, M., Alwasel, SH, Alhazza, IM, Jomova, K., Kollar, V., Rusko, M., & Valko, M. (2019). Ukulawulwa koxinzelelo lwe-oxidative kunye nezinye iipathologies kwi-Alzheimer's disease. Oovimba beToxicology, 93(9), 2491-2513. https://doi.org/10.1007/s00204-019-02538-y
Sridharan, B., & Lee, M.-J. (2022). I-Ketogenic Diet: I-Neuroprotective Composition ethembisayo yokulawula izifo ze-Alzheimer kunye ne-Pathological Mechanisms. Iyeza langoku leMolekyuli, 22(7), 640-656. https://doi.org/10.2174/1566524021666211004104703
Strope, TA, & Wilkins, HM (2023). Amyloid precursor protein kunye ne-mitochondria. Uluvo lwangoku kwi-Neurobiology, 78, 102651. https://doi.org/10.1016/j.conb.2022.102651
Thakur, S., Dhapola, R., Sarma, P., Medhi, B., & Reddy, DH (2023). I-Neuroinflammation kwi-Alzheimer's Disease: Inkqubela phambili yangoku kwi-Molecular Signaling and Therapeutics. Ukuvutha, 46(1), 1-17. https://doi.org/10.1007/s10753-022-01721-1
Varesi, A., Pierella, E., Romeo, M., Piccini, GB, Alfano, C., Bjørklund, G., Oppong, A., Ricevuti, G., Esposito, C., Chirumbolo, S., & UPascale, A. (2022). Indima enokwenzeka ye-Gut Microbiota kwi-Alzheimer's Disease: Ukusuka kwi-Diagnostic ukuya kuNyango. Amanzi, 14(3), 668. https://doi.org/10.3390/nu14030668
Indlela yokuphila yeVascular Dementia kunye neZondlo zoThintelo lweSicwangciso-ProQuest. (nd). Ibuyiselwe nge-27 kaJanuwari 2022, ukusuka https://www.proquest.com/openview/44d6b91873db89a2ab8b1fbe2145c306/1?pq-origsite=gscholar&cbl=18750&diss=y
Wang, J.-H., Guo, L., Wang, S., Yu, N.-W., & Guo, F.-Q. (2022). Iindlela ezinokubakho ze-pharmacological ze-β-hydroxybutyrate zokuphucula imisebenzi yokuqonda. Iingcamango zangoku kwi-Pharmacology, 62, 15-22. https://doi.org/10.1016/j.coph.2021.10.005
Warren, CE, Saito, ER, & Bikman, BT (nd). Ukutya kwe-Ketogenic kuphucula ukusebenza kakuhle kwe-Hippocampal Mitochondrial. 2.
Xu, Y., Zheng, F., Zhong, Q., & Zhu, Y. (2023). Ukutya kwe-Ketogenic njengeNgcaciso ye-Non-Drug Intervention ye-Alzheimer's Disease: Iinkqubo kunye neeMpembelelo zeKlinikhi. Ingxelo yeZifo ze-Alzheimer's, 92(4), 1173-1198. https://doi.org/10.3233/JAD-230002
Yassine, HN, Self, W., Kerman, BE, Santoni, G., Navalpur Shanmugam, N., Abdullah, L., Golden, LR, Fonteh, AN, Harrington, MG, Gräff, J., Gibson, GE, Kalaria, R., Luchsinger, JA, Feldman, HH, Swerdlow, RH, Johnson, LA, Albensi, BC, Zlokovic, BV, Tanzi, R., … Bowman, GL (2023). I-metabolism yesondlo kunye ne-cerebral bioenergetics kwi-Alzheimer's disease kunye ne-dementias ehambelana nayo. Alzheimer kunye nesifo sengqondo esixhalabisayo, 19(3), 1041-1066. https://doi.org/10.1002/alz.12845
Yin, JX, Maalouf, M., Han, P., Zhao, M., Gao, M., Dharshaun, T., Ryan, C., Whitelegge, J., Wu, J., Eisenberg, D., Reiman , EM, Schweizer, FE, & Shi, J. (2016). I-Ketones ivimba ukungena kwe-amyloid kunye nokuphucula ukuqonda kwimodeli ye-Alzheimer. Neurobiology yokwaluphala, 39, 25-37. https://doi.org/10.1016/j.neurobiolaging.2015.11.018
Younes, L., Albert, M., Moghekar, A., Soldan, A., Pettigrew, C., & Miller, MI (2019). Ukuchonga iiNguqulelo kwii-Biomarkers Ngexesha leSigaba se-Preclinical ye-Alzheimer's Disease. Imida kwi-Neuroscience yokuguga, 11. https://www.frontiersin.org/articles/10.3389/fnagi.2019.00074
Yudkoff, M., Daikhin, Y., Nissim, I., Lazarow, A., & Nissim, I. (2004). Ukutya kwe-Ketogenic, ingqondo ye-glutamate metabolism kunye nokulawula ukubamba. Prostaglandins, Leukotrienes kunye ne-Essential Fatty Acids, 70(3), 277-285. https://doi.org/10.1016/j.plefa.2003.07.005
Zhu, H., Bi, D., Zhang, Y., Kong, C., Du, J., Wu, X., Wei, Q., & Qin, H. (2022). Ukutya kwe-Ketogenic kwizifo zabantu: iindlela ezisisiseko kunye nokwenzeka kokuphunyezwa kweklinikhi. UTshintsho loMqondiso kunye noNyango oluJolisiweyo, 7(1), iSiqendu 1. https://doi.org/10.1038/s41392-021-00831-w