A hypothesis of " blood-stasis and toxin causing catastrophe engender acute cardiovascular event (ACE)" was put forward according to TCM cognition on blood-stasis and toxin, in combining with the up to date concept of atherosclerosis and coronary heart disease, and together with our clinical practical experiences. The etiology, pathogenesis, evolving law, initial characteristics, clinical manifestation, therapeutic methods, prescriptions and their compatibility, as well as the well-suited time for applying TCM intervention were discussed. The authors stressed that it is of great significance for further reducing the morbidity of ACE and improving the effect of integrative medicine for preventing and treating cardiovascular thrombotic disease.
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Alzheimers Dement
December 2024
Ivane Beritashvili Center of Experimental Biomedicine, Tbilisi, Georgia.
Background: There is growing evidence from laboratory and clinical trials that deep brain stimulation (DBS) at memory associated structures enhances cognitive functions. Best site for memory enhancing-DBS is still unclear. The medial septum (MS), the important modulator of the hippocampal neural network, might be a key target to accomplish therapeutic efficacy in memory impaired patients.
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December 2024
Yale University School of Medicine, New Haven, CT, USA.
Background: In neurodegenerative disease such as Alzheimer's disease and stroke, the brain transitions to pro-inflammatory profile, where microglia and T-cells in the brain have increase inflammatory profiles, along with increased Kv1.3 potassium channel abundance. Pharmacological blockade of Kv1.
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December 2024
Aligarh Muslim University, Aligarh, UttarPradesh, India.
Background: Following the genome-wide association studies (GWAS) discovery of microglia-specific genes, particularly Trem-2, SHIP-1, and CD33, significantly associated with higher Alzheimer's disease (AD) risk, the microglia TREM2 pathway has become central for regulating amyloid load, tissue damage, and limiting its spread. These discoveries have opened up the exciting possibility of therapeutic microglia TREM2 manipulation in AD. To date, however, several elements of TREM2 signaling remain unknown, ranging from the temporal activation pattern and receptor-ligand binding to modulation of the brain microenvironment.
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December 2024
Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA.
Background: Multiple AD risk genes are implicated in lipid metabolism, and plasma and brain lipid levels are altered in AD. Astrocytes are enriched in key lipid-related factors and are likely contributors to altered lipid homeostasis in AD. We hypothesize that APP/Aβ-related pathology and neuroimmune factors modulate astrocytic gene transcription that promote maladaptive changes in lipid pathways, including aberrant astrocytic production and release of lipids that could affect Aβ pathology and neuronal deficits.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Ivane Beritashvili Center of Experimental Biomedicine, Tbilisi, Georgia.
Background: Alzheimer's disease (AD) is a neurodegenerative disease that causes progressive cognitive decline over age 65. Individuals suffering from this disease suffer memory loss, and histological examination of the brains. Okadaic acid (OA), is a potent and selective inhibitor of protein phosphatases 1 and 2A.
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