"Xiusanzhen" can regulate the expression of hippocampal Bcl-2 and Bax proteins in AD rats, which may contribute to its clinical effect in relieving AD, and the therapeutic effect depends on the integrity of the olfactory nerve pathway.
Bcl-2-associated athanogen 1M (BAG-1M), initially identified as an anti-apoptotic protein, has also been found to be highly expressed in the same neurons that contain intracellular amyloid in the hippocampus of AD patient.
A combined alteration such as up-regulation of S100beta together with down-regulation of Bcl-2 may be important in the pathogenesis of Alzheimer's disease and Down's syndrome.
After the treatment of ZiShen prescription, the expression of Bcl-2 was upregulated, along with a downregulation of Bax in the cortex and hippocampus of compound AD model rats.
Apoptosis, lipid peroxidation and DNA damage were significantly higher after exposure to P(GFLG)-ADR, as reflected by simultaneous activation of p53, c-fos in A2780 cells) or c-jun (A2780/AD) signaling pathways and inhibition of the bcl-2 gene.
Bax, Bcl-2 and TRADD mRNA levels also differed little between case types, although there were small but significant decreases in Bax mRNA levels in AD compared to control cases and Bcl-2 mRNA in AD cases compared to pathologically aged and control cases.
CP alterations in iron contents were mediated through DMT1(-IRE) and changes in ROS levels, which in turn attenuated the progression of AD through the Erk/p38 and Bcl-2/Bax signaling pathways.
However, the expression of bcl-2 was higher in PBMC from SDAT patients than in cells from MID patients or from MISC patients, whereas the MIXED group showed an intermediate expression; a high bcl-2 expression correlated with a low DEX-sensitivity.
In the common DLB forms, nigral bcl-xL and bcl-2 proteins levels were significantly decreased in the DLB cases associated with a concomitant severe AD pathology (p < 0.05).
In this study, we investigated the gene expression of 14 apoptotic genes (E2F1, p21/WAF, ICE-LAP3, Fas Antigen, CPP-32, GADD153, ICE-beta, c-Fos, c-Jun, Bax-alpha, Bcl-2, Bcl-(x)L, BAK, and p53) in 5 normal and 6 AD human hippocampal tissues, using reverse transcription-polymerase chain reaction.
Melatonin significantly ameliorated the cognitive function and mitochondrial damage in AD mice, reduced the expression levels of GSK-3β, caspase-3, Aβ<sub>1-42</sub> , BACE1, p-tau protein and increased the expressions of PP2A and Bcl-2.
Our results suggest that the Bcl-2rs956572 polymorphism is associated with different strengths of structural covariance in AD that determine clinical outcomes.
Taken together, these results demonstrate that genetically disrupting BECN1-BCL2 binding hyperactivates autophagy in vivo, which sequestrates amyloid oligomers and prevents AD progression.
The Aβ<sub>1-42</sub> mice that received E2 treatment during the early stage of AD pathology exhibited significant reductions in the production of nitric oxide (NO) and reactive oxygen species (ROS), a marked decrease in the activation of Cytochrome-c/Bax/Bcl-2/caspase-3 pathway, a notable decrease in the level of gliosis a significant increase in the number of synapses (ultrastructural investigation), and a marked upregulation in synaptic function-related proteins compared to mice that received E2 treatment during the late stage of AD pathology.
The balance of pro- and anti-apoptotic Bcl-2 family proteins (e.g., Bcl-2 and Bcl-w versus Bad, Bim and Bax) has been known to have a role in neuronal cell death and, importantly, expression levels of these proteins are reportedly altered in the vulnerable neurons in AD.
The current investigation focused on detection of PtdSer on the outer leaflet of the bilayer in synaptosomes from brain of subjects with AD and amnestic mild cognitive impairment (MCI), as well as expression levels of apoptosis-related proteins Bcl-2, Bax, and caspase-3.
The current investigation focused on detection of PtdSer on the outer leaflet of the bilayer in synaptosomes from brain of subjects with AD and amnestic mild cognitive impairment (MCI), as well as expression levels of apoptosis-related proteins Bcl-2, Bax, and caspase-3.
The expression levels of B cell lymphoma 2 (Bcl‑2) were increased, and the expression levels of caspase‑3, Bcl‑2 associated X protein and AD‑associated proteins were decreased in the hippocampus following treatment with vildagliptin.