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Biomedical subjects

C Albrecht

Publications and source records attributed to C Albrecht.

At least 19 recordsLinked to original sources
PubMed2006

Placental ABCA1 expression is reduced in primary antiphospholipid syndrome compared to pre-eclampsia and controls.

The ATP binding cassette transporter A1 (ABCA1) mediates cellular cholesterol and phospholipid efflux, and is implicated in phosphatidylserine translocation and apoptosis. Loss of functional ABCA1 in null mice results in severe placental malformation. This study aimed to establish the placental localisation of ABCA1 and to investigate whether ABCA1 expression is altered in placentas from pregnancies complicated by pre-eclampsia and antiphospholipid syndrome. ABCA1 mRNA and protein localisation studies were carried out using in situ hybridization and immunohistochemistry. Comparisons of gene expression were performed using real-time PCR and immunoblotting. ABCA1 mRNA and protein was localised to the apical syncytium of placental villi and endothelia of fetal blood vessels within the villi. ABCA1 mRNA expression was reduced in placentas from women with APS when compared to controls (p<0.001), and this was paralleled by reductions in ABCA1 protein expression. There were no differences in ABCA1 expression between placentas from pre-eclamptic pregnancies and controls. The localisation of ABCA1 in human placenta is consistent with a role in cholesterol and phospholipid transport. The decrease in ABCA1 protein in APS may reflect reduced cholesterol transport to the fetus affecting the formation of cell membranes and decreasing the level of substrate available for steroidogenesis.

ATP Binding Cassette Transporter 1↗
PubMed2006

Degradation of transgenic Cry1Ab DNA and protein in Bt-176 maize during the ensiling process.

Maize silage is commonly used as feed for farm animals. The aim of this study was to monitor the time-dependent degradation of non-recombinant chloroplast DNA (exemplified by the rubisco gene) in comparison with the recombinant cry1Ab gene in the course of the ensiling process. In parallel, the Cry1Ab protein content and fragment sizes were determined. Fragments of the rubisco (173, 896, 1197, 1753 and 2521 bp) and of the cry1Ab gene (211, 420, 727 and 1,423 bp) were selected to investigate the DNA degradation process. The detection of the Cry1Ab protein was performed using an enzyme-linked immunosorbent assay (ELISA) and immunoblotting. Rubisco gene fragments of 173 bp were still detectable after 61 days, while fragments of 1,197 and 2,521 bp were detectable up to 30 days and on the first day only respectively. Polymerase chain reaction (PCR) analyses revealed that fragments of the cry1Ab gene with sizes of 211 and 420 bp were detectable up to 61 days, fragments with sizes of 727 and 1,423 bp, 30 and 6 days respectively. The ELISA showed a decrease of the Cry1Ab protein in maize silage during the ensiling process. No marked degradation was observed during the first 43 h. Thereafter, a sharp decrease was measured. After 61 days, 23.6 +/- 0.9% of the initial Cry1Ab protein was still detectable. Immunoblotting confirmed the results of the ELISA showing a positive signal of approximately 60 kDa size for 8 days of ensiling; no further immunoactive fragments were detectable by immunoblotting. In conclusion, the ensiling process markedly decreases the presence of long functional cry1Ab gene fragments and full size Cry1Ab protein.

Animal Feed↗
PubMed2006

In situ studies on the time-dependent degradation of recombinant corn DNA and protein in the bovine rumen.

An in situ technique was adopted to investigate the time-dependent ruminal degradation of chloroplast compared with recombinant DNA of Bt176 corn using conventional and quantitative PCR assays. In parallel, the Cry1Ab protein content and fragment sizes were determined by ELISA and immunoblotting techniques. Triplicate nylon bags filled with 5 g of each substrate (whole-plant isogenic, whole-plant transgenic, ensiled isogenic, and ensiled transgenic corn) were positioned within the rumen of 5 rumen-cannulated, nonlactating cows and incubated for 2, 4, 8, 16, 24, and 48 h. To investigate the DNA degradation process, PCR assays were developed to detect fragments of the endogenous highly abundant rubisco gene (173, 896, 1,197, and 1,753 bp) and of the recombinant cry1Ab gene (211, 420, 727, and 1,423 bp). Short fragments of rubisco (<431 bp) and cry1Ab DNA (211 bp) were amplifiable in whole-plant and ensiled corn samples incubated in the rumen for 48 h, whereas the traceability of larger fragments depended on previous processing of the sample (whole-plant or ensiled corn), the length of the target sequence, and concomitantly on the length of time incubated in the rumen. Quantification of rubisco and cry1Ab gene fragments applying real-time PCR assays revealed degradation to <20% of initial 0-h values within 2 h and <0.5% after 48 h of ruminal incubation. Analysis of Cry1Ab protein in whole-plant corn using the ELISA technique revealed a decrease to 28.0% of the initial value within 2 h and to 2.6% within 48 h. The concentration of Cry1Ab protein of ensiled corn was only 10% that of whole-plant corn. Ensiled corn Cry1Ab protein decreased to 10% of initial values after 48 h of ruminal incubation. Using an immunoblotting technique, the full-size Cry1Ab protein was only detectable up to 8 h; thereafter, only fragments of approximately 17 and 34 kDa size were found. In conclusion, ruminal digestion decreased the presence of functional cry1Ab gene fragments. It is unlikely that full-size, functional Cry1Ab protein will be present after 8 h of incubation in the rumen. Therefore, results based on ELISA measurements should be interpreted carefully and verified by another detection method that discriminates between the full-size and fragmented Cry1Ab protein.

Animals↗
PubMed2006

Identification of the bovine cholesterol efflux regulatory protein ABCA1 and its expression in various tissues.

The ATP-binding cassette transporter A1 (ABCA1) is known to play a significant role in cellular export of phospholipids and cholesterol in humans. The ABCA1 transporter might also play a crucial role in cellular cholesterol homeostasis in the cow or in the transfer of cholesterol into the milk, but its presence and tissue distribution in the bovine is unknown. Therefore, we studied the expression and distribution of the bovine ABCA1 transporter using quantitative PCR and sequenced the entire ABCA1 coding region. In addition, the proximal promoter was identified and screened for regulatory elements. Concordant with data from other mammalian species, bovine ABCA1 mRNA was expressed and detected in all tissues tested. The highest expression levels were detected in lung, esophagus, uterus, spleen, and muscle. Sequence analysis revealed that the open reading frame of this gene consists of 6,786 bases and encodes for a protein of 2,261 AA with a predicted molecular weight of 254 kDa. The deduced bovine ABCA1 protein shows the highest AA sequence homology with human (94%), mouse (93%), rat (92%), and chicken (85%). Analysis of the putative ABCA1 promoter region revealed potential transcription factor binding sites associated with ABCA1 transcription and lipid metabolism. This work could open new avenues for elucidating a potential role of ABCA1 in sterol homeostasis in the bovine organism.

ATP Binding Cassette Transporter 1↗
PubMed2006

Identification, sequence analysis and mRNA tissue distribution of the bovine sterol transporters ABCG5 and ABCG8.

The family of ATP-binding cassette (ABC) transporters consists of several transmembrane proteins that use ATP hydrolysis as an energy source for the transport of a variety of substances through cellular membranes. Two members of this family, ABCG5 and ABCG8, are implicated in the intestinal absorption and biliar excretion of sterols. Cholesterol content in milk is highly variable among species, breeds, and individuals of the same species, but a potential application of these genes in lipid homeostasis in the mammary gland has never been addressed. In the present work, expression of ABCG5 and ABCG8 in the bovine was demonstrated for the first time and characterized by quantitative PCR. The entire coding region and promoter area were sequenced and screened for motifs involved in lipid homeostasis. Both ABCG5 and ABCG8 presented a high level of length and sequence identity with other mammalian species. In the intergenic promoter region, 2 GATA boxes, a liver receptor homolog-1 response element, and a nuclear factor-kappaB response element, important factors in other lipid regulatory processes, were identified. As expected, high expression levels of both ABCG5 and ABCG8 were present in liver and digestive tract samples, and interestingly, in the mammary gland, opening new avenues for further investigation about their potential role in lipid trafficking and excretion during lactation.

ATP-Binding Cassette Transporters↗
PubMed2005

Dynamic force spectroscopy of the digoxigenin-antibody complex.

Small ligands and their receptors are widely used non-covalent couplers in various biotech applications. One prominent example, the digoxigenin-antibody complex, was often used to immobilize samples for single molecule force measurements by optical trap or AFM. Here, we employed dynamic AFM spectroscopy to demonstrate that a single digoxigenin-antibody bond is likely to fail even under moderate loading rates. This effect potentially could lower the yield of measurements or even obscure the unbinding data of the sample by the rupture events of the coupler. Immobilization by multiple antibody-antigen bonds, therefore, is highly recommended. The analysis of our data revealed a pronounced loading rate dependence of the rupture force, which we analyzed based on the well-established Bell-Evans-model with two subsequent unbinding barriers. We could show that the first barrier has a width of Deltax(1)=1.15 nm and a spontaneous rate of k(off1)=0.015 s(-1) and the second has a width of Deltax(2)=0.35 nm and a spontaneous rate of k(off2)=4.56 s(-1). In the crossover region between the two regimes, we found a marked discrepancy between the predicted bond rupture probability density and the measured rupture force histograms, which we discuss as non-Markovian contribution to the unbinding process.

Antibodies↗
PubMed2005

mRNA expression of genes involved in lipid efflux and matrix degradation in occlusive and ectatic atherosclerotic disease.

BACKGROUND: Atherosclerotic plaque behaviour is influenced by intra-plaque inflammation, matrix turnover, and the lipid core volume. Peroxisome proliferator activated receptor gamma (PPARgamma) modulates atherosclerosis by its anti-inflammatory and anti-protease activity. PPARgamma promotes lipid efflux through the liver X receptor alpha (LXRalpha) and the ATP binding cassette transporter A1 (ABCA1). Matrix metalloproteinase 9 (MMP-9) and cyclooxygenase 2 (COX-2) are implicated in plaque instability. AIMS: To assess the expression of these genes in occlusive and ectatic atherosclerotic disease to determine the relation between genes involved in lipid efflux and matrix degradation. METHODS: Carotid endarterectomy specimens from 16 patients and aneurysm tissue from 16 patients undergoing abdominal aortic aneurysm repair were used. Inferior mesenteric arteries from colectomy specimens from 12 patients served as controls. Total RNA was extracted from pulverised tissue and reverse transcribed into cDNA. Quantitative real time polymerase chain reaction (PCR) was performed using fluorescently labelled probes for ABCA1, LXRalpha, PPARgamma, COX-2, and MMP-9. RESULTS: PPARgamma expression was significantly lower in both occlusive and ecstatic atherosclerotic disease (p<0.001), whereas LXRalpha and ABCA1 expression was significantly increased (p<0.01). MMP-9 expression was significantly increased in diseased tissues (p<0.0001), and values were highest in occlusive disease (p<0.01). The increases in ABCA1 and MMP-9 mRNA were significantly correlated in diseased tissues (p<0.01, r=0.71 and r=0.78). COX-2 expression was increased in ectatic but low in occlusive disease (p<0.01). CONCLUSION: This observational study suggests a role for therapeutic upregulation of PPARgamma, which could potentially upregulate lipid efflux through ABCA1 and inhibit matrix degradation through inhibition of MMP-9.

ATP Binding Cassette Transporter 1↗
PubMed2005

ABCA1 and atherosclerosis.

ATP binding cassette transporter A1 (ABCA1) mediates the cellular efflux of phospholipids and cholesterol to lipid-poor apolipoprotein A1 (apoA1) and plays a significant role in high density lipoprotein (HDL) metabolism. ABCA1's role in the causation of Tangier disease, characterized by absent HDL and premature atherosclerosis, has implicated this transporter and its regulators liver-X-receptoralpha (LXRalpha) and peroxisome proliferator activated receptorgamma (PPARgamma) as new candidates potentially influencing the progression of atherosclerosis. In addition to lipid regulation, these genes are involved in apoptosis and inflammation, processes thought to be central to atherosclerotic plaque progression. A Medline-based review of the literature was carried out. Tangier disease and human heterozygotes with ABCA1 mutations provide good evidence that ABCA1 is a major candidate influencing atherosclerosis. Animal and in vitro experiments suggest that ABCA1 not only mediates cholesterol and phospholipid efflux, but is also involved in the regulation of apoptosis and inflammation. The complex and beneficial interactions between apoA1 and ABCA1 seem to be pivotal for cholesterol efflux. The expression of the ABCA1 is tightly regulated. Furthermore the plaque microenvironment could potentially promote ABCA1 protein degradation thus compromising cholesterol efflux. PPAR-LXR-ABCA1 interactions are integral to cholesterol homeostasis and these nuclear receptors have proven anti-inflammatory and anti-matrix metalloproteinase activity. Therapeutic manipulation of the ABCA1 transporter is feasible using PPAR and LXR agonists. PPAR agonists like glitazones and ABCA1 protein stabilization could potentially modify the clinical progression of atherosclerotic lesions.

ATP Binding Cassette Transporter 1↗
PubMed2004

ABCA1 expression in carotid atherosclerotic plaques.

BACKGROUND AND PURPOSE: The ATP-binding cassette transporter A1 (ABCA1) facilitates cholesterol efflux from cells, a key process in reverse cholesterol transport. Whereas previous investigations focused on mutations causing impaired ABCA1 function, we assessed the role of ABCA1 in human carotid atherosclerotic disease. METHODS: We compared the mRNA and protein levels of ABCA1, and one of its key regulators, the liver X receptor alpha (LXRalpha), between minimally and grossly atherosclerotic arterial tissue. We established ABCA1 and LXRalpha gene expression by real-time quantitative polymerase chain reaction in 10 control and 18 atherosclerotic specimens. Presence of ABCA1 protein was assessed by immunoblotting. To determine whether differences observed at a local level were reflected in the systemic circulation, we measured ABCA1 mRNA in leukocytes of 10 patients undergoing carotid endarterectomy and 10 controls without phenotypic atherosclerosis. RESULTS: ABCA1 and LXRalpha gene expression were significantly elevated in atherosclerotic plaques (P<0.0001 and 0.03, respectively). The increased mRNA levels of ABCA1 and LXRalpha were correlated in atherosclerotic tissue (r=0.85; P<0.0001). ABCA1 protein expression was significantly reduced in plaques compared with control tissues (P<0.0001). There were no differences in leukocyte ABCA1 mRNA expression (P=0.67). CONCLUSIONS: ABCA1 gene and protein are expressed in minimally atherosclerotic human arteries. Despite significant upregulation of ABCA1 mRNA, possibly mediated via LXRalpha, ABCA1 protein is markedly reduced in advanced carotid atherosclerotic lesions. No differences in leukocyte ABCA1 expression were found, suggesting the plaque microenvironment may contribute to the differential ABCA1 expression. We propose that the decreased level of ABCA1 protein is a key factor in the development of atherosclerotic lesions.

ATP Binding Cassette Transporter 1↗
PubMed2004

Leukocyte ABCA1 gene expression is associated with fasting glucose concentration in normoglycemic men.

Adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) mediates the efflux of cholesterol to apolipoprotein A1, a process necessary for high-density lipoprotein (HDL) formation and reverse cholesterol transport. In patients with Tangier disease, mutations in ABCA1 result in low circulating HDL-cholesterol and predisposition to coronary heart disease (CHD). ABCA1 gene expression is decreased in diabetic mice. In humans, glycated hemoglobin (HbA(1c)) predicted future CHD events, even within the normal range. We hypothesised that leukocyte ABCA1 gene expression would be inversely associated with indices of glycemia in normoglycemic men. Fasting blood samples were taken from 32 healthy, nonsmoking, normoglycemic men (age 23 to 46 years). ABCA1, peroxisome proliferator-activated receptor gamma (PPARgamma), and liver X receptor alpha (LXRalpha) gene expressions in circulating leukocytes were measured using TaqMan technology. Significant inverse associations between ABCA1 gene expression and both fasting glucose concentration (r = -0.49, P =.008) and age (r = -0.39, P =.043) were found. There was no association with HbA(1c) (r = -0.23, P =.238) or HDL-cholesterol concentration (r = 0.02, P =.904). In a multiple regression model, fasting glucose remained a significant independent predictor (P =.037), whereas age did not (P =.226). Mechanisms underlying the association were explored; there were no significant associations between fasting glucose concentration and leukocyte PPARgamma gene expression, or between fasting glucose concentration and leukocyte LXRalpha gene expression. This is the first demonstration of an association between ABCA1 gene expression and fasting glucose concentration in vivo.

ATP Binding Cassette Transporter 1↗
PubMed2002

Functional analysis of candidate ABC transporter proteins for sitosterol transport.

Two ATP-binding cassette (ABC) proteins, ABCG5 and ABCG8, have recently been associated with the accumulation of dietary cholesterol in the sterol storage disease sitosterolemia. These two 'half-transporters' are assumed to dimerize to form the complete sitosterol transporter which reduces the absorption of sitosterol and related molecules in the intestine by pumping them back into the lumen. Although mutations altering ABCG5 and ABCG8 are found in affected patients, no functional demonstration of sitosterol transport has been achieved. In this study, we investigated whether other ABC transporters implicated in lipid movement and expressed in tissues with a role in sterol synthesis and absorption, might also be involved in sitosterol transport. Transport by the multidrug resistance P-glycoprotein (P-gp; Abcb1), the multidrug resistance-associated protein (Mrp1; Abcc1), the breast cancer resistance protein (Bcrp; Abcg2) and the bile salt export pump (Bsep; Abcb11) was assessed using several assays. Unexpectedly, none of the candidate proteins mediated significant sitosterol transport. This has implications for the pathology of sitosterolemia. In addition, the data suggest that otherwise broad-specific ABC transporters have acquired specificity to exclude sitosterol and related sterols like cholesterol presumably because the abundance of cholesterol in the membrane would interfere with their action; in consequence, specific transporters have evolved to handle these sterols.

3T3 Cells↗
PubMed2001

Elongated multiple electronic cascade and cyclization spacer systems in activatible anticancer prodrugs for enhanced drug release.

The design and synthesis of several novel elongated self-elimination spacer systems for application in prodrugs is described. These elongated spacer systems can be incorporated between a cleavable specifier and the parent drug. Naphthalene- and biphenyl-containing spacers were synthesized but did not eliminate. Prodrugs of the anticancer agents doxorubicin and paclitaxel are reported that contain two or three electronic cascade spacers. A novel catalytic application of HOBt was found for the synthesis of N-aryl carbamates through reacting a 4-nitrophenyl carbonate with an aniline derivative, to connect the 1,6-elimination spacers via a carbamate linkage. In addition, a double spacer-containing paclitaxel prodrug was synthesized, comprising a 1,6-elimination spacer and a bis-amine linker connected to paclitaxel via a 2'-carbamate linkage. Prodrugs in which the novel spacer systems were incorporated between a specific tripeptide specifier and the parent drug doxorubicin or paclitaxel proved to be significantly faster activated by plasmin in comparison with prodrugs containing conventional spacer systems. It is expected that the generally applicable novel spacer systems reported herein will contribute to future development of improved enzymatically activated prodrugs.

Antineoplastic Agents↗
PubMed2001

Fragments of human oncoprotein MDM2 reveal variable distribution within and on cultivated human hepatoma cells.

Human oncoprotein MDM2 reveals a MHC class I binding motif HMDM441 characterizing MDM2 as a potential tumor antigen. To analyze the distribution of MDM2 proteins containing this motif in liver cancer cells we produced rabbit anti-HMDM441 serum. The novel antibodies bound to an MDM2 fragment of approximately 55 kDa which lacked the N-terminal region and was present in lysate and supernatant of a human hepatoma cell line overexpressing normal 90-kDa MDM2. The 55-kDa fragment was detected in the cytoplasm and nucleoli and at the nuclear envelope of hepatoma cells, whereas normal hepatocytes were negative. Double-fluorescence labeling indicated that the MDM2 fragments and MHC class I molecules were coexpressed on the surface of the hepatoma cells. Further studies must clarify whether MDM2 fragments containing motif HMDM441 are novel targets of immunotherapy and immunochemical tumor diagnosis.

Blotting, Western↗
PubMed2001

Quantum interference in artificial band structures.

Magnetotransport experiments on two-dimensional electron systems with an atomically precise, one-dimensional potential modulation reveal striking quantum interference oscillations. Within a semiclassical framework, they are recognized either as self-interference along closed orbits, many of them rendered possible by magnetic breakdown between Fermi contour segments of the artificial band structure, or as interference-enhanced backscattering. The known commensurability oscillations appear as a special case of the latter mechanism.

Journal Article↗
PubMed2001

Evidence of Hofstadter's Fractal Energy Spectrum in the Quantized Hall Conductance.

The energy spectrum of a two-dimensional electron system in a perpendicular homogeneous magnetic field and a weak lateral superlattice potential with square symmetry is composed of Landau bands with recursive internal subband structure. The Hall conductance in the minigaps is anticipated to be quantized in integer multiples of e(2)/h that vary erratically from minigap to minigap in accordance with a Diophantine equation. Hall measurements on samples with the requisite properties uncover this long searched for evidence of Hofstadter's butterflylike energy spectrum.

Journal Article↗
PubMed2001

[3H]acetycholine release in rat striatal slices is not subject to dopamine heteroreceptor supersensitivity 30 months after 6-hydroxydopamine lesion of the substantia nigra.

Using the rat model of Parkinson's disease described by Ungerstedt the release of [3H]acetylcholine ([3H]ACh) in the caudatoputamen was investigated to assess possible long-term effects of unilateral dopaminergic denervation on the modulation of cholinergic interneurons. This seemed of interest since rats with 6-hydroxydopamine (6-OHDA) lesions of the left substantia nigra showed an increase in the behavioural susceptibility to small doses of dopamine (DA) D2 receptor agonists 30 months after the lesion. Electrical field stimulation with 3 Hz elicited release of [3H]ACh in slices of both the lesioned and the intact striatum. The DA reuptake blocker nomifensine was ineffective on the lesioned side but diminished the release of [3H]ACh in the intact striatum. This inhibition was reversed by the D2 receptor antagonist domperidone and hence probably due to the effect of endogenously released DA. Single electrical pulses at 0.05 Hz, which neither induced autoinhibition of [3H]ACh release nor heteroinhibition by endogenous DA, elicited a higher release of [3H]ACh on the intact side. Under this stimulation paradigm activation of the D2 heteroreceptor with quinpirole depressed the release of [3H]ACh to a similar extent on both sides, irrespective of the absence or presence of the competitive NMDA receptor antagonist D-CPPene. Also blockade of the NMDA receptor channel by dizocilpine, or of AMPA receptors by NBQX, was ineffective on either side. The NMDA-evoked release of [3H]ACh was higher on the lesioned side. It was equally depressed by quinpirole and by ethanol on both sides. Thus, single electrical pulses and NMDA stimulation per se had opposite effects on the lesioned and the intact side, whereas the modulation of release was similar. Since the lesioned striata were considerably smaller, measurements of mRNA levels of choline acetyltransferase (ChAT) were used to assess the density of cholinergic interneurons and their content of ChAT mRNA. This analysis did not reveal any side difference. In conclusion, the function of D2 heteroreceptors on, and the density and ChAT mRNA content of, cholinergic interneurons are not or no longer altered after long-term DA denervation. Most probably, cholinergic interneurons are not involved in the increased behavioural susceptibility of 6-OHDA-lesioned rats to DA agonists.

Acetylcholine↗
PubMed2001

Regulation of gene expression by muscarinic acetylcholine receptors.

In the brain, muscarinic acetylcholine receptors (mAChRs) are involved in higher cognitive functions including synaptic plasticity and memory. In Alzheimer's disease (AD) patients the cholinergic nervous system is severely damaged. In order to reinforce the cholinergic system, clinical tests were started to use cholinomimetic drugs to treat AD patients. To identify the genes involved in mAChR signalling, we used a differential display approach and found 11 genes that were readily activated by mAChR with 1 hour of activation. These included the transcription factors Egr-1, Egr-2, Egr-3, c-Jun, Jun-D and Gos-3; the growth regulator hCyr61; the signalling factors NGFi-B (nerve growth factor induced gene-B) and Etr101; the unknown gene Gig-2 (for G-protein-coupled receptor induced gene 2); and the acetylcholinesterase gene (ACHE). Our data show that multiple immediate-early genes are under the control of mAChRs, and they suggest that these genes play important roles in coupling receptor stimulation to long-term neuronal responses. The results also suggest a feedback mechanism where up-regulated ACHE expression and accelerated breakdown of acetylcholine (ACh) at the cholinergic synapses limits increases in cholinergic transmission. Three hours after m1 mAChR activation a different pattern of gene expression was demonstrated. It included the novel genes Gig-3 and Gig-4, as well as the LIM-only protein LM04. Like ACHE, these genes are target genes which may be under the control of the above immediate-early genes. Together, our data show that muscarinic receptors induce a complex and sustained pattern of gene expression that may be involved in the regulation of cholinergic transmission as well as the control of cellular functions in post-synaptic cholinergic target cells. These results may contribute to a better understanding of the effects and side effects of cholinomimetic treatment in AD patients.

Alzheimer Disease↗