Mechanisms Of Neuroplasticity And Brain Degeneration: Strategies for Protection Thaum Cov Txheej Txheem Kev Laus Part 1

Abstract

Kev laus yog cov txheej txheem dynamic thiab zuj zus uas pib ntawm kev xeeb tub thiab txuas ntxiv mus txog thaum tuag. Cov txheej txheem no txo qis homeostasis thiab morphological, biochemical, thiab kev puas siab puas ntsws hloov pauv, ua rau tus neeg muaj kev cuam tshuam rau ntau yam kab mob.

Raws li peb muaj hnub nyoog, peb lub cim xeeb yuav hloov, uas yog kev zam. Txawm li cas los xij, muaj qee yam uas peb tuaj yeem ua tau los pab peb kom muaj kev nco qab noj qab haus huv thiab ua rau kev laus qeeb.

Ua ntej, nws yog ib qho tseem ceeb kom noj qab haus huv. Kev tawm dag zog ntau tuaj yeem txhim kho cov ntshav ncig, nce oxygen thiab cov as-ham rau lub hlwb, thiab txhim kho kev nco. Peb yuav tsum ua ntau dua aerobic ce, xws li taug kev nrawm thiab ua luam dej, uas pab kom muaj kev noj qab haus huv. Nyob rau tib lub sijhawm, peb kuj yuav tsum tau ua tib zoo saib xyuas peb tus cwj pwm noj mov. Noj zaub thiab txiv hmab txiv ntoo tshiab ntxiv thiab txo cov piam thaj thiab rog tuaj yeem txhim kho kev nco.

Qhov thib ob, peb yuav tsum ua kom peb lub hlwb ua haujlwm. Qhov no tuaj yeem ua tiav los ntawm kev nyeem ntawv ntau ntxiv, kawm, thiab tshawb nrhiav yam tshiab. Kev kawm tsis tu ncua kev paub tshiab thiab kev txawj ntse tuaj yeem txhawb nqa lub hlwb neural network, pab txhim kho kev nco, thiab txhim kho kev txawj ntse. Tsis tas li ntawd xwb, peb kuj tuaj yeem koom nrog qee yam kev ua si, xws li pab pawg kis las, seev cev, thiab ua haujlwm pub dawb, uas tuaj yeem txhawb peb lub hlwb thiab txhim kho peb lub cim xeeb.

Thaum kawg, kev mob siab rau kev sib tw thiab kev nyuaj siab hauv lub neej kuj tuaj yeem pab txhim kho peb lub cim xeeb. Kev ntxhov siab tsim nyog tuaj yeem pab peb tswj xyuas kom pom tseeb thiab ua kom pom tseeb, yog li txhim kho peb lub cim xeeb. Peb yuav tsum lees txais cov kev cov nyom thiab kev nyuaj siab hauv lub neej thiab kawm kom hloov kho thiab kov yeej lawv.

Hauv cov ntsiab lus, peb tsis tas yuav txhawj txog kev poob peb lub cim xeeb vim kev laus. Peb tuaj yeem ncua kev laus thiab txhim kho peb lub cim xeeb los ntawm kev noj qab haus huv, ua kom peb lub hlwb ua haujlwm, thiab teb cov teeb meem thiab kev ntxhov siab. Cia peb ua lub neej zoo thiab ua siab mos siab muag kom peb txoj kev nco yuav noj qab nyob zoo thiab muaj zog. Nws tuaj yeem pom tau tias peb yuav tsum txhim kho peb lub cim xeeb, thiab Cistanche tuaj yeem txhim kho kev nco zoo vim Cistanche yog cov tshuaj suav tshuaj suav nrog ntau yam tshwj xeeb, ib qho ntawm kev txhim kho kev nco. Cov nyhuv ntawm Cistanche los ntawm ntau yam khoom xyaw uas nws muaj, suav nrog tannic acid, polysaccharides, flavonoid glycosides, thiab lwm yam. Cov khoom xyaw no tuaj yeem txhawb nqa lub hlwb kev noj qab haus huv ntau txoj hauv kev.

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Kev loj hlob ntawm cov neeg laus laus tau nce qhov ntau ntawm cov kab mob sib kis, kev puas tsuaj ntawm lub hauv paus paj hlwb, thiab kev dementias, xws li Alzheimer's kab mob, uas nws qhov kev pheej hmoo tseem ceeb yog hnub nyoog, ua rau muaj coob tus neeg uas xav tau kev txhawb nqa txhua hnub. kev ua neej nyob.

Qee qhov kev xav txog kev laus qhia tias mob tshwm sim los ntawm kev nce ntawm cellular senescence thiab reactive oxygen hom, uas ua rau mob, oxidation, cell membrane puas, thiab li ntawd neuronal tuag.

Tsis tas li ntawd, mitochondrial kev hloov pauv, uas tau tsim tawm thoob plaws hauv cov txheej txheem kev laus, tuaj yeem ua rau muaj kev hloov pauv hauv kev tsim hluav taws xob, tsis muaj hluav taws xob thauj khoom, thiab apoptosis induction uas tuaj yeem ua rau txo qis kev ua haujlwm.

Tsis tas li ntawd, nce cellular senescence thiab tso tawm ntawm proinflammatory cytokines tuaj yeem ua rau muaj kev puas tsuaj rau cov neuronalcells. Cov ntawv ceeb toom tsis ntev los no taw qhia txog qhov tseem ceeb ntawm kev hloov pauv txoj kev ua neej los ntawm kev ua kom lub cev muaj zog, txhim kho kev noj haus, thiab kev txhawb nqa ib puag ncig kom qhib cov txheej txheem neuroprotectivedefense.

Yog li, qhov kev tshuaj xyuas no yog txhawm rau hais txog cov ntaub ntawv tshiab tshaj plaws txog cov txheej txheem sib txawv ntsig txog neuroplasticity thiab neuronal tuag thiab muab cov tswv yim uas tuaj yeem txhim kho neuroprotection thiab txo cov neurodegeneration los ntawm kev laus thiab ib puag ncig kev ntxhov siab.

Lo lus tseem ceeb: cell senescence; cell signaling; cholinergic; enriched ib puag ncig; lub sij hawm ntev; neurodegeneration; neurogenesis; neuroinflammatory; neuronal tuag; neuroprotection; neurotrophin.

Taw qhia

Ib qho ntawm cov lus nug tseem ceeb tshaj plaws nyob rau hauv neuroscience yog hais txog kev nkag siab txog cellular thiab molecular xwm txheej cuam tshuam nrog kev tuag neuronal tom qab mob hnyav, xws li ashypoxia, ischemia, epileptogenic crises, thiab hypoglycemia, thiab hauv cov xwm txheej ntev, xws li cov kab mob neurocognitive loj. Cov kab mob neurodegenerative xws li Alzheimer's disease. , amyotrophic lateral sclerosis (Rybakowski et al., 2018) thiab Parkinson's disease yog pathologies yam ntxwv los ntawm lawv cov kev puas tsuaj rov qab los ntawm qee cov neurons thiab kev vam meej thiab tsis muaj peev xwm poob ntawm qee yam haujlwm ntawm lub paj hlwb (Ntxuam thiab al., 2017) thiab yog qhov tseem ceeb ntawm dementia.

Cov kab mob neurodegenerative yog tshwm sim los ntawm cov noob caj noob ces (kev hloov pauv ntawm cov kab mob cuam tshuam nrog cov noob) thiab ib puag ncig (xws li cov teebmeem ntawm kev laus thiab kev ua neej) kev sib cuam tshuam (Herrero andMorelli, 2017).

Cov kab mob no muaj cov yam ntxwv xws li kev ua haujlwm tsis zoo ntawm lub cev, excitotoxicity, misfolded protein aggregation, tsim cov kab mob oxidative reactive (ROS), mitochondrial dysfunction, intracellular calcium dysregulation, thiab cell poob (Fan li al., 2017).

Kev cuam tshuam ntawm tes ua haujlwm, nrog rau kev puas tsuaj DNA ntau ntxiv thiab kev laus-txhim kho oxidativestress, maj mam ua haujlwm tiv thaiv kab mob, suav nrog kev tswj hwm cov protein zoo (xws li, ubiquitination thiab autophagy) thiab lwm yam, ua rau muaj kev tuag ntawm tes (apoptosis) (Hollville li al., 2019).

Ntau txoj hauv kev yuav muaj feem cuam tshuam nrog kev tuag ntawm tes ua ib feem ntawm cov txheej txheem kev laus vim muaj cov kab mob neurodegenerative. Celldeath tej zaum yuav tshwm sim los ntawm stimuli los ntawm lub cell nws tus kheej los yog los ntawm toxicfactors uas qhib cell tuag txoj kev uas muaj xws li excitotoxicity, oxidative kev nyuaj siab, thiab tso tawm ntawm senescence-associated secreted phenotypes (SASPs).

Txawm hais tias tag nrho cov xwm txheej no yuav tshwm sim raws li ib feem ntawm txoj kev laus, tam sim no tau pom tseeb tias txoj kev ua neej tuaj yeem ua rau muaj kev tiv thaiv kev tiv thaiv uas tuaj yeem hloov pauv txoj kev laus. Cov no suav nrog kev ua si ntawm lub cev (Andel li al., 2016), kev noj zaub mov kom txaus raws li cov khoom noj muaj calorie tsawg (Wahl li al., 2016), kev txhawb siab rau ib puag ncig (Balthazar et al., 2018), thiab qib ntawm kev txawj ntse tau txais los ntawm kev kawm txuj ci. (Soldan li al., 2017; Balduino et al., 2020).

Feem ntau ntawm cov tswv yim no tau raug pov thawj tias ua tau zoo hauv kev tsim lub hlwb kom ncua lossis tiv thaiv kev loj hlob ntawm ntau hom kev dementia hauv cov neeg laus.

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Hauv kev tshuaj xyuas no, peb piav qhia txog cov txheej txheem ntsig txog toneuroplasticity thiab neurodegeneration thiab lub luag haujlwm ntawm cell senescence hauv cov txheej txheem degenerative thiab cell tuag. Peb kuj tham txog kev ua tau zoo ntawm ntau lub tswv yim uas yuav tsim kev tiv thaiv lub hlwb thiab ua kom lub neej zoo nyob rau hauv cov laus.

Tshawb nrhiav lub tswv yim thiab cov txheej txheem xaiv

Tshawb nrhiav cov ntaub ntawv pov thawj tau ua nyob rau hauv USNational Library of Medicine ntawm National Institutesof Health (PubMed.gov). Cov ntaub ntawv pov thawj ntawm 2015 thiab 2019 tau nyiam siv tshwj tsis yog cov ntaub ntawv qub xav tau. Cov ntsiab lus siv raws li kev tshawb fawb yog: neuroplasticity, neurodegeneration, neuroprotection, thiab hlwb laus.

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Neuroplasticity yog lub peev xwm ntawm lub hlwb hloov mus tas li thoob plaws hauv ib tus neeg lub neej thiab tuaj yeem pom ntawm ntau theem, nrog rau kev coj cwj pwm thiab kev kawm thiab kev nco nyob rau saum toj ntawm hierarchy, txuas cov qauv kev hloov pauv nrog kev ua haujlwm.

Lub hauv paus ntawm lub pyramid no yog tsim los ntawm cov molecules thiab lawv cov kev sib cuam tshuam, uas muaj cov synapses, neuronal circuits, thiab ntau theem ntawm kev khi (Daim duab 1). Synapses yog qhov chaw tshwj xeeb ntawm cov hlwb neuronal uas sawv cev rau cov qauv tseem ceeb cuam tshuam nrog cov tshuaj neurotransmission hauv lub paj hlwb.

Anelementary txoj cai ntawm neuroplasticity yog morphological hloov pauv ntawm synaptic kev sib txuas uas yog tas li renewedor recreated, nrog rau qhov sib npaug ntawm cov txheej txheem no yog nyob ntawm kev ua haujlwm neuronal (Jasey thiab Ward, 2019).

Kev ua haujlwm-raws li kev hloov pauv hauv synapses yog ib qho ntawm cov ntsiab lus tseem ceeb ntawm lub tswv yim ntawm neuroplasticity thiab kev kawm thiab kev nco txoj kev xav raws li kev paub txog kev tsim cov engrams, lub cev cov cim ntawm kev hloov pauv hauv cov qauv synaptic (Jasey thiab Ward, 2019). Raws li kev nco consolidation tuaj yeem raug ntaus nqi rau cellular thiab molecularprocesses uas ua rau cov neuron hloov nws cov lus teb rau ib qho kev txhawb nqa.

Qhov tshwm sim no muaj feem cuam tshuam ncaj qha rau toreater synaptic kev ua tau zoo los ntawm electrophysiologicalalteration hu ua long-term potentiation (LTP), muaj peev xwm ntawm consolidating morphological thiab functional alterations insynapses nyob rau lub sij hawm ntev, nrog rau cov kev hloov ntawm cov noob caj noob ces thiab protein synthesis (Petsophonsakul et 07).

Cov xwm txheej molecular koom nrog hauv neuroplasticity tuaj yeem muab faib ua cov qauv (neurogenesis thiab dendritic spineformation) thiab ua haujlwm (hloov hauv kev tso tawm cov tshuaj chemicalmediators, receptor rhiab heev, thiab ua kom cov postsynapticmechanisms) (Kulik li al., 2019). yog hippocampal neurogenesis.

Qhov tshwm sim no yog tsim los ntawm plaub theem sib txawv: kev loj hlob, kev tsiv teb tsaws, qhov sib txawv, thiab kev loj hlob (Kempermann li al., 2018).Lub cellular precursor pom nyob rau hauv lub hippocampus, tshwj xeeb tshaj yog nyob rau hauv lub subgranular cheeb tsam ntawm lub dentate gyrus (Volianskis 205 etal.), ib hom astrocyte uas qhia txog cov cim tseem ceeb ntawm kev loj hlob ntawm tes xws li glial fibrillary acid protein, proliferating cell nuclear antigen thiab nestin (Kempermannet al., 2018).

Tom qab cov txheej txheem ntawm kev faib cell, feem ntau cov hlwb raug apoptosis los yog phagocytized los ntawm microglia (Li andBarres, 2018). Ciaj sia nyob neuroblasts nres kev nthuav qhia cellproliferation-txog cov proteins thiab pib qhia cov structuralproteins xws li doublecortin; txij li lub sijhawm ntawd, kev sib koom ua ke ntawm kev qhia ntawm doublecortin, neuronal nuclearprotein, calretinin, thiab calbindin characterizes tus txheej txheem ntawm cellular sib txawv (Kempermann li al., 2015).

Cov neurons tshiab no tau paub tab hauv thaj tsam granular ntawm thedentate gyrus thiab yog excitatory glutamatergic neurons. Theneurogenesis ntawm cov hlwb yog tswj los ntawm neurotrophin theem xws li hlwb-derived neurotrophic factor (BDNF). Yog li, stimuli uas cuam tshuam nrog BDNF ntau lawm thiab kev ua si kuj cuam tshuam rau cov neeg laus hippocampal neurogenesis (Zhang li al., 2018).

Cov kev hloov pauv hloov pauv hauv lub synaptic structural complex yog tswj hwm los ntawm kev sib cuam tshuam ntawm lub davhlau ya nyob twg presynaptic, thaj av postsynaptic, thiab astrocytes, hu ua tripartite synapses. Perisynaptic astrocyte cov txheej txheem ua lub luag haujlwm tseem ceeb hauv kev ruaj khov thiab kev loj hlob ntawm dendritic spines, cuam tshuam cov kev hloov pauv ntawm cov neuroplasticity (Haroon li al., 2017; Li thiab Barres, 2018).

Astrocytes expressmetabotropic thiab ionotropic receptors, uas tuaj yeem ua haujlwm los ntawm cov neurotransmitters (norepinephrine, acetylcholine, thiab glutamate) tso tawm. Nyob rau hauv txoj kev no, astrocytes tuaj yeem hloov pauv, tso cai rau lawv tshawb xyuas thiab hloov kho lub zog ntawm synapticactivity (Verkhratsky thiab Nedergaard, 2018).

Qhov nce hauv Ca2+ qib hauv astrocytes nyob ntawm qhov kev ua haujlwm neuronal thiab ua rau muaj kev tso tawm ntau lub gliotransmitters (ATPand glutamate) hauv synapse, muab ntau txoj hauv kev los tswj kev ua haujlwm synaptic (Rusakov, 2015; Bazargani thiab Attwell, 2016).

Tsis tas li ntawd, astrocytes yog nplua nuj nyob rau hauv transporters forglutamate, glycine, thiab -aminobutyric acid, uas yog siv los tshem tawm lawv los ntawm cov synaptic cleft thiab, los ntawm enzymes, los hloov lawv mus rau hauv precursors thiab ces, nyob rau hauv pre-synapticterminals, reconverting rau active transmitters.

Yog li, astrocytes pab txhawb rau neuroprotection, raws li lawv khaws cov qib ntawm extra-synaptic glutamate tsawg los tiv thaiv excitotoxicity.

Hauv qhov no, cov ntaub ntawv qhia tau hais tias astrocytes tuaj yeem zais ntau cytokines thiab chemokines, xws li interleukin 1 (IL-1), IL6, chemokine CXC motif ligand-1, IL-8, nuclear factor-kappaB , interferon - -induced protein 10, qog necrosis factor-, CC motif ligand chemokine, macrophage inflammatoryprotein 1 alpha, macrophage migration inhibitory factor, andgranulocyte-macrophage colony-stimulating factor, ua rau infiltration ntawm circulating leukocytes rau lub hlwb thiab inflammatory txheej txheem, uas tej zaum yuav tshwm sim los ntawm perivascular kev ua ntawm lub microglia (Lian thiab Zheng, 2016; Liebner li al., 2018). Kev ua kom tsis tu ncua ntawm glial hlwb ua rau mob tuaj yeem yog cov lus teb neurotoxic uas tuaj yeem cuam tshuam nrog kev loj hlob ntawm cov kab mob neurodegenerative (Osborn li al., 2016; Kawano li al., 2017).

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Yog li, raws li cov lus teb rau ntau hom kev thuam xws li ischemia, kev raug mob, thiab cov kab mob neurodegenerative xws li Alzheimer's kab mob, astrocytes tau txais kev hloov pauv ntawm cov cellular thiab molecular uas ua rau muaj kev hloov pauv hloov pauv mus rau kev hloov pauv synaptic plasticity.

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Ntawm cov kev hloov pauv molecular, ob lub tshuab standout: lub glutamatergic thiab cholinergic. Nyob rau hauv glutamatergicsystem, N-methyl-D-aspartate (NMDA) receptors yog qhov tseem ceeb ntawm cov kev ua haujlwm-dependent synaptic plasticity uas koom nrog hauv kev txawj ntse xws li kev kawm thiab kev nco (Volianskis li al., 2015).

NMDA receptor hasa di- lossis tri-heteromeric qauv thiab yuav tsum muaj ob lub GluN1 subunits txuam nrog GluN2 subunits ora sib xyaw ntawm GluN2 thiab GluN3.

Hauv hippocampus, muaj qhov tseem ceeb ntawm cov qauv heteromeric nrog GluN1-N2A thiab GluN1-N2B subunits. Raws li txhua tus GluN2 subunitconfers cov cim qhia txog kev hloov pauv cov peev txheej, tau muaj kev xav tias qhov muaj pes tsawg leeg ntawm NMDAR subunit ua rau LTP lossis kev nyuaj siab ntev (LTD).

Hauv Alzheimer's tus kab mob, siab ntom ntom ntawm -amyloidplaques nyob rau hauv hippocampus paub tias yuav ua rau muaj kev hloov pauv ntawm NMDA Glu-N2A subunits nrog Glu-N2B (viacalpains) pab txhawb kev sib khi rau SAP -102, uas nthuav tawm kev txav mus los ntxiv rau thaj tsam ntxiv (synaptic). Parsonsand Raymond, 2014; Zhang thiab al., 2016).

Yog li, es tsis txhob NMDA-R2B nyob rau hauv sab hauv los ntawm endocytosis rau kev rov ua dua, nws yuav nthuav dav ntxiv tom qab mus rau qhov chaw ntxiv-synaptic, uas yog qhov chaw tseem ceeb ntawm txoj kev taw qhia, ua rau apoptotic neuronal tuag (ntawm caspase-3) (Parsons thiab Raymond. , 2014; Zhang thiab al., 2016; Bading, 2017). Tsis tas li ntawd, cov ntaub ntawv qhia tau hais tias cov khoom noj muaj protein ntau PSD-95 bindsto cytoskeleton proteins cuam tshuam rau kev sib txuas ntawm synaptic, nrog rau kev tswj cov synapse architecture thiab morphology (de Wilde li al., 2016); Yog li ntawd, nws yog ib qho tseem ceeb rau synapticstabilization thiab receptor kev tswj kev khiav tsheb, los ntawm recruitment ntawm receptors los ntawm qhov chaw ntxiv-synaptic mus rau active zone tomodification ntawm intracellular signaling proteins.

Qhov tseem ceeb ntawm cholinergic system rau LTP modulationand induction yog qhia nyob rau hauv cov kev tshawb fawb yav dhau los qhia tias nyob rau hauv presynaptic neurons lub 7 cholinergic receptor inducesthe synthesis thiab tso tawm ntawm cov neurotransmitters koom nrog tsim LTP, xws li glutamate, raws li tau tham saum toj no (Lozada li al., 2012; Haam thiab Yakel, 2017) (Daim duab 2).

Hauv postsynaptic neurons, tib receptor ua rau ntawm Ca2+ / calmodulin-dependent protein kinase txoj hauv kev, qhov twg membrane-derived Ca2+ permeability ua rau cov protein kinaseA ua kom thiab ua rau CREB phosphorylation, uas yog lub luag haujlwm rau kev tswj cov protein synthesis. xav tau kom ruaj khov cov kev hloov pauv synaptic uas tshwm sim thaum kawm (Daim duab 2).

Nws cov haujlwm yog tswj hwm los ntawm phosphorylation, feem ntau hauv Ser133, los ntawm ntau cov proteins, ntawm lawv CAMKIV, uas ua raws li cov tshuaj calmodulin effector thiab induces anincrease nyob rau hauv kev tso tawm ntawm cov proteins sib txawv, xws li matureBDNF, uas tom qab kev cuam tshuam nrog nws cov receptor tshwj xeeb tropomyosin receptor kinase B nyob rau hauv lub postsynaptic membrane, ua nws lub luag haujlwm tseem ceeb txog kev loj hlob thiab qhov sib txawv ntawm cov neurons tshiab thiab kev loj hlob thiab kev ua kom zoo ntawm dendritic branching (Beeri thiab Sonnen, 2016; Haamand Yakel, 2017).

Cov kev txhawb nqa no txuas cytoskeletalproteins xws li cov integrin-actin complexes rau postsynapticdendrites, thiab cov kev hloov hauv qhov system no hloov qhov ceev ntawm dendritic spicules (Lei li al., 2016; Kulik li al., 2019).

Yog li, kev sib cuag ntawm axons thiab dendrites yog nce thiab ua rau morphological thiab / lossis neurotransmission hloov pauv hauv thesynapses.The alpha7 cholinergic nicotinic receptor plays lub luag haujlwm tseem ceeb hauv neuroplasticity, neuroprotection, thiab nco rov qab nyob rau hauv ob qho tib si noj qab haus huv thiab kab mob. Tsis ntev los no, peb pawg neeg tshawb fawb tau pom tias cov tshuaj tiv thaiv kev tiv thaiv ntawm tus neeg txais kev tiv thaiv kev nco rov qab hauv cov nas xa mus rau qhov kev sim qauv ntawm neurodegeneration ua raws li kev cob qhia, raws li lub tswv yim kom rov qab nco (TellesLongui li al., 2019).

Kev ua kom 7 receptor ua rau muaj kev nce hauv phosphorylation ntawm cov protein kinase Akt, raws li cov receptor muaj peev xwm ua kom phosphoinositide 3-kinase (PI3K) los ntawm Janus kinase 2, uas ua rau inactivation ntawm glycogen synthase kinase 3 thiab nce ntxiv. Bcl-2, ua rau muaj kev tiv thaiv kab mob. Kev ua kom txoj hauv kev PI3K / Akt kuj tuaj yeem tshwm sim los ntawm kev khi ntawm BDNFand NGF neurotrophins rau lawv cov receptors.

Aktphosphorylation thiab ua kom cov cell ciaj sia, inhibition ntawm pro-apoptotic phem protein, thiab ua kom cov ĸĸB kinase inhibitor, inhibiting NF-ĸB tsim (Lee, 2015).

Kev koom tes ntawm BDNF hauv neuroplasticity yog qhov tseem ceeb tshwj xeeb hauv kev hloov pauv ntawm cov qauv thiab kev ua haujlwm synaptic (Sasi et al., 2017; Kowianski li al., 2018), qhov twg BDNFpositively tswj cov synthesis ntawm cov proteins koom nrog kev hloov pauv (Leal et 25, 2018). Cov pov thawj ntxiv ntawm qhov tseem ceeb ntawm BDNF yog pom nyob rau hauv lub xub ntiag ntawm noneurotrophin nyob rau hauv presynaptic glutamatergic neurons (Sasi etal., 2017).

BDNF cuam tshuam cov txheej txheem ntawm neurogenesis hauv thedentate gyrus uas nyiam tsim cov glutamatergic neurons (Leal li al., 2015; Haam thiab Yakel, 2017), ntxiv qhov tseem ceeb ntawm nws lub luag haujlwm hauv ob qho tib si cov qauv thiab kev ua haujlwm neuroplasticity.

Ntxiv rau lub luag haujlwm tseem ceeb uas BDNF plays inneuroplasticity, lwm cov neurotrophins kuj pab txhawb los ntawm kev hloov cov txheej txheem no. Ib qho piv txwv yog insulin-zoo li growthfactor 1 (IGF-1), uas muaj peev xwm ntawm modulating glutamatergicreceptors (Dyer li al., 2016).

Qhov kev loj hlob no cuam tshuam nrog AMPA receptor viability, txhawb clathrin-mediatedendocytosis, thiab ua IGF-1 ib qho tseem ceeb LTD modulator.Ntxiv rau, IGF-1 zoo nkaus li ua kom cov txiaj ntsig ntawm glutamatergic synapses los ntawm kev tswj cov voltage-dependentCa{{4 }} channels (Dyer et al., 2016; Herrera li al., 2019).

IGF-1 kuj tseem koom nrog hauv PI3K/Akt txoj kev ua kom, ua rau anintracellular cascade muaj peev xwm txhawb nqa cell ciaj sia taus thiab neuroprotection (Bianchi li al., 2017; Wrigley li al., 2017). Thaum kawg, IGF-1 nce TRKB receptor qhia, ua kom yooj yim rau kev khi rau BDNF (Li et al., 2013).

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Mechanisms ntawm NeurodegenerationNecrosis

Cell tuag los ntawm necrosis yog tus cwj pwm los ntawm cov txheej txheem pathological vim tias thaum ua haujlwm, nws txhawb kev ua haujlwm ntawm lub cev. Hom kev tuag no tuaj yeem tshwm sim nyob rau hauv cov xwm txheej hnyav xws li hypoxia, ischemia, intoxication, kev siv yeeb tshuaj, thiab autoimmune cov tshuaj tiv thaiv ntawm cov neeg nyob ib puag ncig (Vanden Berghe li al., 2014; Zhang etal., 2017).

Cov plasma membrane puas, uas ua rau poob ntawm cellular tiv thaiv, nce cytoplasmicand mitochondrial ntim, thiab extravasation ntawm intrato extracellular cov ntsiab lus (Lalaoui li al., 2015).

Qhov kev hloov pauv hauv kev cai lij choj ntawm lub xov tooj ntawm tes ua rau muaj kev cuam tshuam, nrog rau kev ua kom lub cev tiv thaiv kab mob xws li aslymphocytes, macrophages, ILS, thiab transcription factor (TNF) (Zhang li al., 2017).

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