Article ; Online: Medicinal Herbs and Their Derived Ingredients Protect against Cognitive Decline in In Vivo Models of Alzheimer's Disease.
International journal of molecular sciences
2022 Volume 23, Issue 19
Abstract: Alzheimer's disease (AD) has pathological hallmarks including amyloid beta (Aβ) plaque formation. Currently approved single-target drugs cannot effectively ameliorate AD. Medicinal herbs and their derived ingredients (MHDIs) have multitarget and ... ...
Abstract | Alzheimer's disease (AD) has pathological hallmarks including amyloid beta (Aβ) plaque formation. Currently approved single-target drugs cannot effectively ameliorate AD. Medicinal herbs and their derived ingredients (MHDIs) have multitarget and multichannel properties, engendering exceptional AD treatment outcomes. This review delineates how in in vivo models MHDIs suppress Aβ deposition by downregulating β- and γ-secretase activities; inhibit oxidative stress by enhancing the antioxidant activities and reducing lipid peroxidation; prevent tau hyperphosphorylation by upregulating protein phosphatase 2A expression and downregulating glycogen synthase kinase-3β expression; reduce inflammatory mediators partly by upregulating brain-derived neurotrophic factor/extracellular signal-regulated protein kinase 1/2-mediated signaling and downregulating p38 mitogen-activated protein kinase (p38 MAPK)/c-Jun N-terminal kinase (JNK)-mediated signaling; attenuate synaptic dysfunction by increasing presynaptic protein, postsynaptic protein, and acetylcholine levels and preventing acetylcholinesterase activity; and protect against neuronal apoptosis mainly by upregulating Akt/cyclic AMP response element-binding protein/B-cell lymphoma 2 (Bcl-2)-mediated anti-apoptotic signaling and downregulating p38 MAPK/JNK/Bcl-2-associated x protein (Bax)/caspase-3-, Bax/apoptosis-inducing factor-, C/EBP homologous protein/glucose-regulated protein 78-, and autophagy-mediated apoptotic signaling. Therefore, MHDIs listed in this review protect against Aβ-induced cognitive decline by inhibiting Aβ accumulation, oxidative stress, tau hyperphosphorylation, inflammation, synaptic damage, and neuronal apoptosis in the cortex and hippocampus during the early and late AD phases. |
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MeSH term(s) | Acetylcholine ; Acetylcholinesterase/metabolism ; Alzheimer Disease/metabolism ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/metabolism ; Antioxidants/therapeutic use ; Apoptosis Inducing Factor/metabolism ; Brain-Derived Neurotrophic Factor/metabolism ; Caspase 3/metabolism ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/etiology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Glucose/adverse effects ; Glycogen Synthase Kinases ; Humans ; Inflammation Mediators/therapeutic use ; JNK Mitogen-Activated Protein Kinases/metabolism ; Plants, Medicinal/metabolism ; Protein Phosphatase 2/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; bcl-2-Associated X Protein/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism |
Chemical Substances | Amyloid beta-Peptides ; Antioxidants ; Apoptosis Inducing Factor ; Brain-Derived Neurotrophic Factor ; Cyclic AMP Response Element-Binding Protein ; Inflammation Mediators ; bcl-2-Associated X Protein ; Glycogen Synthase Kinases (EC 2.7.11.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Acetylcholinesterase (EC 3.1.1.7) ; Protein Phosphatase 2 (EC 3.1.3.16) ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Caspase 3 (EC 3.4.22.-) ; Glucose (IY9XDZ35W2) ; Acetylcholine (N9YNS0M02X) |
Language | English |
Publishing date | 2022-09-25 |
Publishing country | Switzerland |
Document type | Journal Article ; Review |
ZDB-ID | 2019364-6 |
ISSN | 1422-0067 ; 1422-0067 ; 1661-6596 |
ISSN (online) | 1422-0067 |
ISSN | 1422-0067 ; 1661-6596 |
DOI | 10.3390/ijms231911311 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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