A detailed description of this cognitive and neurobiological prof

A detailed description of this cognitive and neurobiological profile has been elusive, due to a combination of both state-and Abiraterone manufacturer trait-related changes in bipolar disorder. In principle, three distinct profiles may exist. An abnormality may be a state-related deficit that recovers fully during periods of remission, but

is similarly affected by both manic and depressive episodes. We have presented evidence that executive dysfunction may adhere to this profile, associated with reduced neural activation in the dorsal and lateral aspects of the prefrontal cortex. However, it should be noted that executive Inhibitors,research,lifescience,medical dysfunction in bipolar disorder is heterogeneous, and this deficit, can persist in some patients, probably as a function of clinical features such as illness severity and possibly medication status. The second profile of deficit, is the trait marker: an impairment that is present during acute episodes but, which also persists during periods of remission. There is reasonable

evidence Inhibitors,research,lifescience,medical that deficits in target detection on sustained attention (CPT) tasks adhere to a trait profile. Trait deficits may occur as a consequence Inhibitors,research,lifescience,medical of repeated illness episodes (as may be the case for executive dysfunction), or may predate the onset, of the illness and be associated with genetic liability Inhibitors,research,lifescience,medical to bipolar disorder. Ongoing research in high-risk populations, such as the unaffected first-degree relatives of bipolar probands, may identify neurocognitive markers

associated with bipolar vulnerability, but studies so far have been inconclusive and limited by small sample sizes.107-109 The third profile is of a state-related marker that is restricted to either the manic or the depressive episodes. We have presented some evidence that deficits in risk assessment, emotional decision-making, and impulsive responding Inhibitors,research,lifescience,medical are pronounced during the manic episodes, and these may represent objective, quantifiable indicators of the classic manic symptoms of disinhibition and behavior with harmful consequences (eg, spending sprees and sexual indiscretions). It is likely that, these deficits are linked to dysregulation 3-mercaptopyruvate sulfurtransferase of the orbitofrontal cortex. The degree to which these changes are restricted to mania is equivocal currently, given the lack of data in bipolar depression. Functional imaging studies in bipolar depression have indicated a hyperreactivity of subcortical limbic systems, such that emotionally neutral material may be processed in an emotional manner. Whilst, it is promising that this phenomenon may show specificity to bipolar disorder compared with major depressive disorder,87 it is not, yet fully clear whether this effect, is restricted to bipolar depression or could represent, a trait marker.

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The biomarker advantage of pramipexole, however, did not translat

The biomarker advantage of pramipexole, however, did not translate into a clear, clinically meaningful advantage. Indeed, although patients

on pramipexole had a lower incidence of complications, patients randomized to initial levodopa had an early and sustained improvement in function, and less somnolence and edema. In the ELLDOPA trial15 during which three increasing doses Inhibitors,research,lifescience,medical of levodopa were compared with placebo in patients with early Parkinson’s disease not requiring dopaminergic therapy, discordant results were noted between the clinical outcomes and the neuroimaging end point. Analysis of the 123I-b-CIT outcome suggested a trend toward a. more rapid decline in striatal dopamine transporter in individuals on the highest doses of levodopa, Inhibitors,research,lifescience,medical but the largest, clinical improvement, was observed in the levodopa. group, in the direction opposite to what would be predicted on the basis of the imaging marker. These results corroborate those of the CALM-PD trial, and indicate that the SPECT 123I-b-CIT biomarker advantage did not translate into a clinically meaningful Inhibitors,research,lifescience,medical advantage. Studies using 18F6-fluoro-L-dopa (F-dopa) positron emission tomography (PET) as a surrogate outcome of Parkinson’s

disease treatment, show similar negative results. The accumulation of these radioactive dopamine metabolites within the striatum, and evidence Inhibitors,research,lifescience,medical correlating their reduction with clinical and pathologic measures,16-18 make F-dopa PET a potential surrogate outcome for treatment assessment. In the REAL PET trial, 2 years after starting treatment, a. 13% decline in F-dopa uptake was seen in the ropinirole group compared with a. 20% decline in the levodopa group.19 However, patients treated with levodopa had significantly greater functional improvement and fewer side effects (excepting dyskinesia), suggesting that F-dopa PET did not, meet criteria for a surrogate outcome of treatment, efficacy. Additional Inhibitors,research,lifescience,medical concerns regarding the

ability to utilize PET as a. marker of therapeutic find more efficacy come from studies evaluating the safety and efficacy of fetal tissue transplantation.20-22 In these studies, a significant, increase in F-dopa uptake was demonstrated in patients receiving fetal Fossariinae tissue transplantation. Regrettably, functional improvement, was not, clearly established, and a significant proportion of treated subjects in both studies developed disabling dyskinesias. This is a. clear example of a case where unexpected consequences of an intervention, not detected by a potential surrogate outcome, resulted in patient harm. The negative results of these trials have raised questions regarding the use of biomarkers in Parkinson’s disease. How can drugs affect, a. biomarker that suggests a.

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Targeting drug-loaded liposomes, in addition to enhancing their

Targeting drug-loaded liposomes, in addition to enhancing their therapeutic activity, enhances tumor detection and response monitoring when they are coloaded

with an imaging agent. Addition of transferrin to 10B plus iodine contrast agent coloaded liposomes allowed a 3.6-fold higher 10B concentration in tumor tissues over untargeted coloaded liposomes [375]. The selective retention of transferrin-targeted formulations led to better tumor detection 72h after administration of liposomes, a period during which the signal from untargeted liposomes had washed out, thus combining monitoring of drug delivery and tumor response with boron neutron capture Inhibitors,research,lifescience,medical therapy [375]. Combined delivery of Gd and doxorubicin in liposomes targeted with a neural cell adhesion Inhibitors,research,lifescience,medical molecule-specific peptide allowed higher concentration of doxorubicin in tumor tissues corCytoskeletal Signaling inhibitor related with increased tumor growth inhibition over untargeted coloaded liposomes together with better visualization of tumors by MRI [392]. Targeting of iron oxide and doxorubicin coloaded liposomes to pancreatic tumors by conjugation of an antimesothelin antibody improved the antitumor activity and tumor signal enhancement over untargeted liposomes [393]. Folate targeting of doxorubicin-loaded liposomes encapsulating iron oxide Inhibitors,research,lifescience,medical resulted in superior tumor growth inhibition of liver cancer tumors than the standard formulation Doxil and simultaneously allowed

tumor imaging by MRI with higher sensitivity than the commercial contrast agent, Resovist [394]. 9. Conclusions In addition to the need for extended blood Inhibitors,research,lifescience,medical circulation and stimuli-controlled extravasation to the tumor’s niche, multifunctional liposomal nanocarriers must target at least one hallmark of cancer (aberrant cell growth, drug resistance, sustained angiogenesis, and tissue invasion) for enhancement of tumor therapy and/or diagnosis. As described throughout the paper, this requires coordinated action

of stealth, targeting, and internalizing Inhibitors,research,lifescience,medical moieties to achieve intracellular delivery to cancer cells in tumors. Moreover, combined targeting of tumor cells and related neoangiogenesis is becoming a focus of research that allows destruction of both primary and unless distant tumor nodules. However, targeted therapies rely on ligands presented by a few types of tumors and must face up to the fact of the heterogeneity of tumor cells and their surface markers [175, 395, 396]. A possible direction may be the coupling of ligands of different natures (antibody, protein, peptides and chimiokine, hormone analogs) to target at least two tumor cell populations for relapse-free cancer therapy and more sensitive malignant lesion detection. Conflict of Interests The authors declare that they have no conflict of interests. Acknowledgments This work was supported by the NIH Grant U54CA151881 to V. P. Torchilin. The authors are grateful to W. C. Hartner for critical review of the paper.

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Louis, MO), was made up to four different concentrations (0 1, 1,

Louis, MO), was made up to four different concentrations (0.1, 1, 10, and 100 μmol/L) in aCSF and kept frozen until use. The solutions were delivered through an electrical syringe pump (Instech, Plymouth Meeting, PA) calibrated to deliver a total volume of 1 μL over 12.5 min. The experiment consisted of a baseline recording (1 h) and an infusion period, after which evoked responses were recorded for an additional 3 h following termination of infusion. Histological Inhibitors,research,lifescience,medical assessment of placements, and data analysis Upon termination of recording, anesthetized animals were decapitated

and the brains were removed quickly and frozen for cryostat sectioning. Coronal sections (30 μm) were taken and electrode placements were visualized using cresyl violet staining and glycogen phosphorylase histochemistry, as described by Walling et al. (2007). Animals in which electrode or cannula Inhibitors,research,lifescience,medical placement occurred outside the dentate gyrus were excluded from analysis. DataWave software was used to measure the population spike amplitude (first positive peak − first valley) and fEPSP Inhibitors,research,lifescience,medical slope (ΔV/Δt) for each waveform recorded. The average value for the last 30 min of baseline recording

was used to see more evaluate changes in both population spike amplitude and fEPSP slope for the duration of recording. Measurements were normalized to the mean of the population spike amplitude or fEPSP slope measurement for the 30-min period prior to infusion onset and transformed into 5-min means. Within-group Inhibitors,research,lifescience,medical analyses Repeated measures analysis of variance (ANOVA) was used to evaluate the effects of intrahippocampal application of ISO on population spike amplitude and fEPSP slope at each of the concentrations (aCSF, 0.1, 1, 10, 100 μmol/L × time). If significant effects were found, further post hoc analyses were carried out using Fisher’s test for Least Significant Differences (LSD) to characterize the differences. Effects were considered significant

if the 5-min means after the start of the infusion were significant (P < 0.05) from Inhibitors,research,lifescience,medical all (6) 5-min means in the 30-min baseline period. A minimum of two consecutive mean calculations were required to be statistically different from baseline. Significance was set at P < 0.05. Between-group analyses Two-way repeated measures ANOVAs (groups: aCSF, 0.1, 1, 10, 100 μmol/L × times: 15 min preinfusion and 15, 110, and 180 min postinfusion) were used to assess below differences in the effects among varying concentrations of ISO. Again, LSD analysis was employed when the interaction was found to be significant and the criteria level was set at a minimum of P < 0.05. Correlations and input/output curves Pearson product–moment correlations were calculated across all animals in each group for the natural variations in slope–spike relationships at the same time points analyzed in the between-group tests (15 min preinfusion and 15, 110, and 180 min postinfusion). A two-tailed test of significance (P < 0.05) was employed.

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This study also highlights the type of thought that should go int

This study also highlights the type of thought that should go into determining the evaluation for a study. Since minor depression was an unknown entity at the time, one of the key questions was: how stable is this entity over time? Although 4 weeks is an arbitrary length of time, we felt for ethical

and scientific reasons, that it would be an adequate length of time for an extended MEK inhibition placebo run-in. Conclusions A careful and critical review of clinical trial methodologies is imperative for the field to move forward. Attention to many of the assumptions that are inclusively made when a trial is designed will be critical in enhancing the success of clinical trials. We must think closely about the diagnostic criteria Inhibitors,research,lifescience,medical used in the trial in the inclusion and exclusion criteria. Many of the currently accepted criteria limit the generalizability of the findings and have not been demonstrated in a systematic fashion to enhance differentiation of drug versus placebo responses. Yet, some important aspects Inhibitors,research,lifescience,medical of the very definition of these syndromes have been neglected, in particular, the importance of including functional disability and quality of

life dysfunction as part of the definition of the syndrome. Some individuals may present with a requisite number of symptoms, Inhibitors,research,lifescience,medical but may not be as adversely affected as if they had had a profound, long-lasting syndrome. It is quite likely they are suffering from a transient constellation of symptoms due to an external stressor. A second Inhibitors,research,lifescience,medical important concern is the appropriateness of the assessments that are being used in randomized controlled trials. Very often, the assessments that are employed represent “me too” assessments, because studies done by other companies have used the measures

in the past. Yet, this may not reflect our best knowledge about, the disorder being studied, nor a sufficient way of bringing a new compound onto the market. Frequently, the argument for the use of such instruments is that they are supposedly mandated by regulatory agencies. However, more often than not, this is a myth that is perpetuated rather than the outcome Inhibitors,research,lifescience,medical of frank and careful discussions with the regulatory authority. A third important issue that requires some thought is assumptions about about the stability of the syndrome over time. Many times, studies are designed with the assumption that randomization to placebo should lead to a relatively static or, if anything, disadvantageous course for patients. Yet, investigation of most medical syndromes suggests that there is an intrinsic waxing and waning to the course of the syndrome. Therefore, arbitrary assessment using instruments that investigate only one aspect of the syndrome may well lead to spurious results. A last concern, but one that can greatly influence a trial, involves appropriate statistical design. Often studies are powered based on desire, rather than available data.

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Selecting patients for more intense radiation therapy will requir

Selecting patients for more intense radiation therapy will require a better understanding of the biology of tumors that tend to recur locally as opposed to distantly and the deployment of techniques to achieve this intensification of radiation therapy safely and effectively. Judicious use of IORT for borderline resectable/unresectable pancreatic cancer patients will ideally be confined to

Inhibitors,research,lifescience,medical patients who (I) receive induction chemotherapy, consolidation chemoradiation, and surgical resection, where possible; (II) undergo prospective collection of selleck inhibitor biomarkers (clinical, radiographic, biochemical or molecular) predictive of local-dominant biology; and (III) are monitored prospectively for toxicity. Vigilance for unique Inhibitors,research,lifescience,medical toxicities of IORT, for instance, was instrumental in identifying more pronounced mammographic changes in the tumor bed (increased calcifications and increased fat necrosis) as a result of IORT following lumpectomy for breast cancer (11). We also envision such studies requiring the concerted effort of a consortium of centers that have IORT capabilities and expertise with pancreatic cancer management, possibly under the auspices of the American College of Surgeons

Oncology Group (ACOSOG) and/or the International Society of Intraoperative Radiation Therapy (ISIORT). Acknowledgements Disclosure: Inhibitors,research,lifescience,medical The authors declare no conflict of interest.
The majority of pancreatic tumours are primary. Pancreatic metastases are rare (3,8% of pancreatic lesions) (1), and are more commonly Inhibitors,research,lifescience,medical reported

in patients with renal cell carcinoma. Metastases of ovarian cancer to the pancreas are very rare but have been reported in the literature (2). We report a very unusual case of a metachronous pancreatic metastasis from an ovarian cancer occurred 8 years after the first diagnosis. Case report We describe a 70 year-old Caucasian female with a prior history (8 years previously) of bilateral hysteroannesiectomy Inhibitors,research,lifescience,medical because of ovarian and uterine serous papillary adenocarcinoma poorly differentiated G3 (pT1c, N0), that presented with jaundice. Her past medical history revealed 4-Aminobutyrate aminotransferase hypertension, Wegener Granulomatosis and bronchial asthma. Laboratory test results included the following: bilirubin 10.1 mg/dL (normal 0.3-1.2 mg/dL); alanine aminotransferase 478 IU/L (0-40 IU/L); alkaline phosphatase 2667 IU/L (70-290 IU/L); γGT 2853 IU/L (0-50 IU/L); Ca19-9 35,3 U/mL (0.0-37 IU/mL); CA 125 90,8 U/mL (0.0-35 IU/mL). Abdominal ultrasound revealed common bile duct (CBD) dilation (20 mm diameter) with concomitant dilatation of intrahepatic biliary tree. The abdominal CT scan showed a 2.5 cm × 3 cm hypodense pancreatic head lesion involving the portal vein (Figure 1). Figure 1 Contrast enhanced CT scan of the abdomen revealing 2.

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While technological advances in capacity for sequencing analysis

While technological advances in capacity for sequencing analysis have exceeded the benchmark measure of computing

power, Moore’s Law, there is no doubt that this success has been largely tied to computational advances. The transfer of this knowledge from the laboratory to the health care setting faces a steep climb to establish information management practices in the US. Improved clinical knowledge from research is highly dependent on recovering standardized, useful clinical information from medical practice. The delivery of knowledge in clinically useful formats to support decision-making processes is similarly critical. The information management needs to Inhibitors,research,lifescience,medical span these gaps is found in the electronic health information technology (health IT). The major components of a health IT system to support personalized Inhibitors,research,lifescience,medical medicine includes widely used electronic medical record systems and personal health records that consumers can use for recording their own health care information. A second component is a nationwide effort to enable health information exchange among health care providers Inhibitors,research,lifescience,medical and institutions that will enable portability of information to suit purposes on demand. A third element

includes electronic decision support capabilities that engage medical records systems to facilitate evidence-based health care choices by the health care provider. Collectively, these are dependent on data standards that Inhibitors,research,lifescience,medical enable semantic and syntactic interoperability of data across health IT systems. As a health care enterprise,

the US has a dearth of electronic information to support these needs, and it will take many years to achieve all of these steps to benefit all patients. The inability to connect information sources is a major contributor to the high costs of clinical research, particularly clinical trials. Despite escalating health care costs and substantial service inefficiencies in the US, there has been little incentive until recently to make capital investments in information Inhibitors,research,lifescience,medical systems for the Akt inhibitor inpatient and ambulatory care setting. Etomidate Today, less than 20% of all physicians use electronic health record systems, and far fewer have systems that provide decision support capabilities to aid personalized medicine. Some progress is being made on the requirement for electronic transmission of prescriptions from the health care provider to the pharmacy. Computerized physician order entry (CPOE) for ordering laboratory tests and other services has also been improving. As part of the American Recovery and Reinvestment Act of 2009, nearly $20 billion will be invested in the next several years to build health IT capacity through network capabilities, support acquisition of electronic systems by practice groups and health care institutions, and provide fiscal incentives for adoption and use of health IT systems.

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Andreasson et al89 prospectively followed up a cohort of Swedish

Andreasson et al89 prospectively followed up a cohort of Swedish conscripts who had been interviewed about their cannabis use at age 18 to 20 years and found an elevated relative risk (RR) for schizophrenia amongst users compared to nonusers (RR=2.4). In 2002, Zammit et al reanalyzed and extended the data,90 and found that the association between selfreported cannabis misuse and later risk of schizophrenia persisted after adjustment for other drug use and personality factors. Also in 2002, Arseneault et al presented their findings from Dunedin on a prospective association between adolescent cannabis use and later psychosis.11 Inhibitors,research,lifescience,medical Those using

cannabis by the age of 15 years later showed more schizophrenia symptoms than controls and were four times more find more likely

to be diagnosed with schizophreniform disorder, even after psychotic symptoms at age 11 were controlled for (although the latter finding was reduced below significance Inhibitors,research,lifescience,medical after adjustment). In addition to these two studies, there have now been another Inhibitors,research,lifescience,medical three large-scale longitudinal investigations in Israel,91 New Zealand,92 and the Netherlands93 all demonstrating a link between cannabis use and later psychosis. Two recent reviews have drawn together the evidence from Inhibitors,research,lifescience,medical these longitudinal studies.94,95 Both conclude that the current evidence has implications for public health messages targeted particularly at vulnerable young people. Arseneault et al94 calculate that, while on an individual level cannabis use is associated with a

twofold increase in RR for schizophrenia, elimination of such use on a population level would reduce the incidence of schizophrenia by approximately 8%. Recent evidence Inhibitors,research,lifescience,medical from a Dutch first-onset study also indicates that cannabis use can precipitate an earlier onset of illness and, in fact, they found such use to be a stronger determinant of early onset than gender.96 Male cannabis users were a mean of 6.9 years younger at illness onset than male nonusers. Thus, there now appears to be increasing evidence that cannabis can trigger the onset of schizophrenia, at least in those who are already predisposed to develop Resminostat the disorder. Whether cannabis misuse can trigger such illness onset in those not previously vulnerable is still contentious. Dopamine dysregulation has long been thought central to generation of psychotic symptoms. Evidence for the hypothesis originally derived from the observation that antipsychotics block dopamine receptors while agonists elicit positive symptomatology More recently the development of psychosis has been postulated to depend on dopamine sensitization.

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Conclusions The ACA training programme appears to be applicable t

Conclusions The ACA training programme appears to be applicable to GPs and GPTs. Future research should assess the effectiveness of the ACA training programme with regard to GP(T) behaviour as well as patient outcomes. Competing interests The funding bodies had no involvement in or influence on the study, and there are no conflicts of interests to be declared. Ethics committee The study protocol was approved by the Medical Ethics Inhibitors,research,lifescience,medical Committee of the VU University Medical Center. Funding body The GP study was funded by the Comprehensive Cancer Centres of Amsterdam and Eindhoven, CZ Healthcare Insurances, Pfizer bv, and the Janivo Foundation. The

GPT study was funded by the Dutch Foundation for the Vocational Training of General Practitioners. Pre-publication history The pre-publication history for this paper Inhibitors,research,lifescience,medical can be accessed here: http://www.biomedcentral.com/1472-684X/11/9/prepub Acknowledgements We wish to thank all the GPs and

GPTs who Roxadustat order participated in this study.
It is commonly believed that 75% Inhibitors,research,lifescience,medical of patients with cancer will have pain at some point in their disease process and that adequate pain management can be achieved through simple measures in 85−95% of cases [1,2]. However, at least 40% of cancer patients are reported to receive inadequate analgesia [3,4]. Palliative Care Teams (PCTs) provide care, including Inhibitors,research,lifescience,medical pain management in acute-care hospitals during the early course of the disease, in conjunction with other life-prolonging therapies, such as chemotherapy or radiation therapy. PCTs facilitate collaboration among specialists and the early

introduction of palliative care services. It has been reported that accurate pain assessment by physicians is associated with improved outcomes for pain management [5-8]. In addition; early referral to palliative care is an important indicator of the quality of care for pain management [9]. Therefore, we hypothesized that early referral to a PCT would be associated with accurate pain assessment by primary physicians. Inhibitors,research,lifescience,medical In previous studies, the barriers to pain assessment have been examined from a variety of perspectives, including barriers related to patients and health care professionals [10]. The most significant barrier was a patient’s most inability to report pain owing to dementia, delirium, and depression [11]. Physician-related barriers may result from insufficient knowledge of palliative care [12]. However, these studies were conducted between primary physicians and oncologists, excluding palliative care physicians [13,14]. Although palliative care physicians have more opportunity to assess cancer patient pain in an inpatient setting, to our knowledge, few studies have compared the specific barriers to accurate pain assessment between primary and palliative care physicians.

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Therapeutic strategies for chronic prophylactic dosing, analogous

Therapeutic strategies for chronic prophylactic dosing, analogous to lipid-lowering treatments for heart disease, are needed to prevent cognitive decline and the development of dementia in patients at the beginning stages of Alzheimer’s disease. This strategy has been relatively effective in the management of cardiovascular disease and may prove a successful strategy for preventing the development

of dementia from Alzheimer’s disease as well. Approaches for interventional treatment The only drugs currently on the market for AD provide primarily symptomatic relief. While the identification of surrogate biomarkers and novel imaging technologies provides the framework to identify Inhibitors,research,lifescience,medical high-risk individuals or individuals with early stage disease pathology, parallel approaches are also needed to develop disease Sepantronium Bromide order modifying drugs to effectively treat these individuals. In terms of AD pathogenesis, it is thought that Aβ aggregation Inhibitors,research,lifescience,medical into amyloid plaques is the causative agent that initiates the disease cascade, leading to Inhibitors,research,lifescience,medical neurofibrillary tangles and neuronal cell loss. This hypothesis has

become known as the amyloid cascade hypothesis.7 This hypothesis was strengthened by human genetic studies identifying mutations in the APP gene in inherited familial early onset AD.26-28 These mutations stimulate APP processing, resulting in increased Aβ42 production. By this hypothesis, therapies capable of reducing Aβ42 levels or preventing its aggregation may block Inhibitors,research,lifescience,medical the disease cascade, making this approach extremely attractive as an early-stage disease intervention. In addition to Aβ-targeted therapies, other therapeutic strategies that would protect neurons from injury are discussed

below. This discussion is by no means a comprehensive list of ongoing treatment research programs, but is meant to highlight some of the key areas that are potentially applicable to preventative treatment development. Inhibitors,research,lifescience,medical There are many research programs dedicated to disrupting Aβ pathology, including directly inhibiting Aβ aggregation, enhancing Aβ clearance, or blocking its production. Inhibiting Aβ aggregation has proven quite challenging; however, many groups are continuing to work on developing small molecule inhibitors of this reaction.29 Investigators are targeting to a wide range of mechanisms to promote the Florfenicol clearance of Aβ from the brain. Included in this are research programs aimed at activating the efflux pumps at the blood-brain barrier, upregulating Aβ degradation enzymes, and immunotherapy methods that target disease-specific Aβ species, among other strategies.30-32 There are also numerous efforts focused on reducing Aβ production by targeting the enzymes that generate Aβ from its precursor, APP.

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