Absstract of: US20260177566A1
The present invention comprises a method for determining the biological age of an animal, wherein the method comprises determining the level of at least one biomarker in said animal, and wherein the at least 1 biomarker is selected from the biomarkers as listed in Table 1.
Absstract of: WO2026136613A1
The present invention relates to methods for treating an ophthalmic condition in a defined patient in need of treatment thereof. The methods comprise inducing the activity of peroxisome proliferator–activated receptor gamma coactivator-1 alpha (PGC1α) in a defined patient that needs treatment of an ophthalmic condition. The defined patient in these methods has been previously identified as having reduced carboxylesterase 1 (CES1) activity, compared to normal activity levels of CES1.
Absstract of: US20260177555A1
0000 The present disclosure relates to a method of separating, purifying, detecting, measuring, or analyzing a sample using a liquid chromatography.
Absstract of: US20260177567A1
The present invention comprises a method for determining the biological age of an animal, wherein the method comprises determining the level of at least one biomarker in said animal, and wherein the at least 1 biomarker is selected from the biomarkers as listed in Table 1.
Absstract of: US20260176315A1
Use of an interleukin 27 (IL-27) protein in preparation of a product for treating and/or delaying Alzheimer's disease (AD) is provided, belonging to the technical field of biomedicine. The IL-27 protein refers to a recombinant IL-27 protein targeting a therapeutic target IL-27, and is selected from the group consisting of a mouse-derived IL-27 protein and a human-derived IL-27 protein, as well as a mammalian IL-27 protein other than the mouse-derived IL-27 protein and the human-derived IL-27 protein. The recombinant IL-27 protein can effectively alleviate the AD caused by Aβ deposition, and can selectively bind to a target receptor, thereby ensuring an accuracy of test results. The protein receptor is highly expressed in the dentate gyrus region of hippocampus, and guarantees drug targeting to the greatest extent.
Absstract of: US20260176332A1
0000 The present application relates to a marker and a method for detecting inflammation-related diseases. The marker of the present application can stably exist in an ex vivo body fluid sample and does not gather on a cell membrane, so the detection result is very accurate. The marker can be widely applied to the medical detection of inflammation-related diseases, having good clinical application prospects.
Absstract of: WO2026134722A1
The present invention relates to a PTEN oxidative inactivation inducer comprising 1,1-diethoxyethane as an active ingredient and use thereof. More specifically, the present invention relates to: a PTEN oxidative inactivation inducer comprising 1,1-diethoxyethane (1,1-DEE) as an active ingredient; and use thereof, for example, a pharmaceutical composition, a cosmetic composition, a food composition, or a feed composition, as a composition for preventing, treating or ameliorating diseases requiring the oxidative inactivation of PTEN, and a method for detecting PTEN redox state.
Absstract of: WO2022118944A1
The present invention addresses the problem of providing: a method for evaluating dementia; and a composition for preventing or treating deterioration in brain function, or maintaining or improving brain function. The intestinal microflora of healthy people, people with mild cognitive impairment, or patients suffering from Alzheimer's disease were compared. As a result, a microorganism belonging to the genus Faecalibacterium was selected as an intestinal microorganism associated with cognitive function. Furthermore, it has been found that Faecalibacterium prausnitzii having a specific DNA exhibits an effect of ameliorating brain function deterioration such as learning and memory impairment.
Absstract of: AU2024406255A1
Compositions and methods are disclosed herein for the treatment of Alzheimer's disease with allogeneic mesenchymal stem cells. The methods of treatment involve the administration of a composition of allogeneic mesenchymal stem cells to a subject in need thereof, wherein the efficacy of the treatment methods can be determined through the measurement of specific biomarkers and improved cognitive function and/or quality of life.
Absstract of: US20260177562A1
Methods of measuring the amount of singly- or multiply-phosphorylated p217+ tau protein in a sample are provided. Methods of detecting or diagnosing tauopathies, methods of determining the effectiveness of a treatment of a tauopathy, and methods of determining whether a subject is suitable for anti-p217+ tau antibody therapy are also provided. Also described are antibodies for use in the methods and kits comprising the antibodies.
Absstract of: US20260176652A1
0000 In certain embodiments the present invention provides a method of treating hearing loss comprising: (a) administering a gene suppression agent that suppresses both copies of an endogenous gene causing the hearing loss; and (b) administering an exogenous wild-type allele engineered to resist suppression by the gene suppression agent. 0000 The present invention provides in certain embodiments a method of treating a genetic hearing loss (GHL) in a patient in need thereof comprising: (a) identifying a mutation in a GHL-causing gene, wherein the mutation causes GHL in the patient; and (b) administering to the patient a pharmaceutical composition comprising a therapeutic miRNA and a pharmaceutically acceptable carrier, wherein the GHL therapeutic miRNA is of 18 to 25 nucleotides in length and knocks-down the GHL-causing gene function at a higher level than it knocks-down gene function in a corresponding wild-type gene.
Absstract of: WO2026135697A1
Patients suffering from, or at risk of developing the symptoms of, Alzheimer's disease and related neuroinflammatory-based diseases, are treated by apheresis to selectively withdrawal Galectin-3 from the patient's body. A reduction in the circulating level of gal-3 of the patient of at least 30% of the patient's pre-treatment galectin-3 level should be sufficient to reduce AD symptoms, and/or inhibit AD progression. A greater withdrawal, up to at least 20%, has greater impact. Selective withdrawal of Galectin-3 may be coupled with the administration of MCP to further slow the progress of, and/or reverse, AD symptoms.
Absstract of: DE102024139461A1
Die vorliegende Erfindung betrifft ein Verfahren zur Herstellung eines In-vitro-Modells für eine neurologische Erkrankung des Menschen. Darüber hinaus betrifft die Erfindung das gemäß dem hierin offenbarten erfindungsgemäßen Verfahren hergestellte In-vitro-Modell. Außerdem betrifft die Erfindung die Verwendung des In-vitro-Modells der Erfindung bei Arzneimitteltests. Darüber hinaus betrifft die Erfindung Verfahren zum Testen der Wirksamkeit von Arzneimitteln bei der Vorbeugung, Verzögerung und Linderung einer neurologischen Erkrankung des Menschen.
Absstract of: US20260177563A1
0000 Disclosed is a sample analyzer comprising: a measurement unit configured to measure an analyte related to a dementia biomarker contained in a sample collected from a subject, the measurement unit comprising: a sample dispenser configured to aspirate the sample from a sample container and discharge the aspirated sample into a cuvette, a first reagent dispenser configured to aspirate a first reagent from a first reagent container and discharge the aspirated first reagent into the cuvette, wherein the first reagent immunologically reacts with the analyte, a second reagent dispenser configured to aspirate a second reagent from a second reagent container and discharge the aspirated second reagent into the cuvette, wherein the second reagent generates light corresponding to an amount of the reacted analyte, a detector configured to detect the generated light from a mixture of the sample, the first reagent, and the second reagent in the cuvette; a controller comprising a processor and programmed to obtain a measurement value of the analyte based on the light detected by the detector; a storage configured to store a reference value that specifies an outlier that may be caused by a factor other than dementia; and an output unit, wherein the controller is programmed to execute a determination on whether the measurement value is specified as the outlier based on the measurement value and the reference value, generate an analysis result of the dementia biomarker based on the mea
Absstract of: WO2026132413A1
The present invention relates to an antibody or antigen-binding fragment thereof, which binds to TDP-43, i.e. TAR DNA-binding protein 43, and to therapeutic and diagnostic uses thereof.
Absstract of: WO2026132444A1
The present invention relates to in vitro methods for diagnosing or prognosing diseases and disorders associated with altered orexin-A levels. It further relates to in vitro methods for monitoring the effect of a treatment or the evolution of a disease or disorder associated with altered orexin-A levels. It also relates to the use of orexin-A fragment as biomarker for the in vitro diagnosis of diseases and disorders associated with altered orexin-A levels.
Absstract of: WO2026134539A1
The present invention relates to a DNA aptamer specifically binding to an alpha-synuclein protein and uses thereof. Specifically, the present invention relates to a DNA aptamer selected from the group consisting of nucleotide sequences of SEQ ID NOS: 1 to 12 and binding specifically to an α-synuclein protein, and a composition for detecting an α-synuclein protein, a detection kit, a detection chip or a microarray, all comprising the aptamer as an active ingredient. In addition, the present invention relates to a method for detecting an α-synuclein protein, a method for providing information for diagnosing a degenerative brain disease, a composition for diagnosing a degenerative brain disease, and a pharmaceutical composition for preventing or treating a neurodegenerative disease, all using the DNA aptamer of the present invention.
Absstract of: US20260177560A1
A process for determining an extent of a central nervous system (CNS) specific neurological condition in a subject including collecting a biological sample of biofluid from the subject and measuring a quantity of a first biomarker, or metabolite of or mRNA corresponding to, the first biomarker from the sample from a dried spot or through a microfluidic device. The biofluid is capillary blood or saliva, which affords ease of collection advantages that are attractive for field-, hospital-, and home-based environments. The process being useful in the diagnosis, care, and management of brain specific abnormal neurological conditions in general, and in particular, to traumatic brain injury (TBI) and (TBI-induced) Alzheimer's disease (AD) and Alexander disease, in which a GFAP mutation is implicated in white matter deterioration.
Absstract of: US20260176364A1
0000 The invention relates to compositions and methods for producing and using antibodies against the alpha7 nicotinic acetylcholine receptor.
Absstract of: US20260177546A1
The invention provides a method for predicting the susceptibility of a patient suffering from a cancer or a myeloid-mediated disease to immunotherapy. Furthermore, the invention provides a method for treating a patient suffering from a cancer or a myeloid-mediated disease with immunotherapy. In accordance with these embodiments, the inventive method includes assaying myeloid cells obtained from the patient prior to treatment for the expression of CXCR3. The invention also provides a genetically engineered myeloid cell (GEMy) in which the expression of CXCR3 is modulated (up- or down-regulated). The invention further provides a composition comprising the inventive GEMy and a pharmaceutically acceptable carrier. The invention also provides a method for treating a patient in need of immunotherapy comprising administering the inventive composition to a patient.
Absstract of: DE102024139033A1
Die Erfindung betrifft ein Peptid, umfassend eine Aminosäuresequenz X6X7X8X9X10X11X12gemäß SEQ ID NO: 1, oder dessen pharmakologisch akzeptable Salze, Derivate und/oder Konjugate, wobei X6ist G oder A, X7ist R oder A, X8ist R oder A, X9ist T oder A, X10ist R oder A, X11ist L oder A, X12ist C oder A, mit der Maßgabe, dass eine der Aminosäuren an Position X6, X7, X8, X9, X10, X11oder X12Alanin sein kann, wobei das Peptid eine Gesamtlänge im Bereich von 7 bis 30 Aminosäuren aufweist, und wobei ein Peptid bestehend aus der Aminosäuresequenz KRRPAKAWSGRRTRLCC gemäß SEQ ID NO: 2 ausgenommen ist. Die Erfindung betrifft ferner Arzneimittel umfassend ein Peptid gemäß SEQ ID NO: 1 sowie eine Verwendung zur Herstellung eines Arzneimittels.
Absstract of: WO2026134051A1
This plasmalogen detection method comprises: a sample preparation step for mixing a Schiff's reagent and a specimen containing a plasmalogen to obtain a sample; a reaction step for reacting the plasmalogen in the sample with the Schiff's reagent; and a contact step for bringing at least some of the sample reacted in the reaction step into contact with a stationary phase containing a silica gel.
Absstract of: WO2025040574A1
Alzheimer's disease is strongly linked to biological aging and bioenergetic abnormalities. Systemic dysregulation of metabolism is a hallmark of the physiological decline of tissues with age. We aimed to explore untargeted metabolomic profiling of blood samples from amyloid-positive people to distinguish individuals who progressed to cognitive decline from those who remained cognitively intact despite having amyloid deposits in the brain. A minimal signature of 9 metabolites identified decliners and non-decliners of cognitive function in participants with an amyloid load. These findings are of clinical importance as they suggest that a metabolic fingerprint may help to predict patients who will develop cognitive decline. Due to the high prevalence of brain amyloid-positivity in older adults, identifying adults who will have cognitive decline will enable the development of personalized and early interventions. The present invention relates to an in vitro method for predicting cognitive decline in a subject comprising the step of determining the level of at least one metabolite selected in the group consisting of 3-hydroxybutyrate, acetone, triglyceride 48:3, glucose, citrate, succinate, methionine, serine, sphingomyelin d18:1/C26:0 in a biological sample obtained from the subject.
Absstract of: EP4764499A1
0001 The present invention relates to a method of detection of glycated proteins, particularly gHSA, which comprises the steps of: i) providing anthracene boronic acid methacrylate (ABAM): 10-N-methyl-N-(o-boronobenzyl)aminomethyl-anthracene-9-methyl methacrylate; ii) preparing a solution of ABAM in a biocompatible buffer with pH in the range of from 6.5 to 8.5 or in in vitro blood plasma sample of a healthy subject; iii) measuring initial fluorescence intensity of ABAM solution from step ii) at the wavelength of from 410 to 520 nm; iv) in vitro mixing of a known amount of ABAM solution from step ii) with a known amount of biological sample; v) measuring fluorescence intensity of the mixture from step iv) at the wavelength of from 410 to 520 nm; vi) determining the fluorescence intensity increases between the initial control fluorescence intensity measured in step iii) and the fluorescence intensity of the mixture of ABAM and biological sample measured in step v); vii) calculating the amount of glycated proteins in the biological sample. 0002 The present invention further relates to the use of this method in determination of the total concentrations of glycated proteins, particularly gHSA, in plasma samples and diagnostics for diabetes mellitus.
Nº publicación: EP4762363A1 24/06/2026
Applicant:
JANSSEN PHARMACEUTICA NV [BE]
Janssen Pharmaceutica NV
Absstract of: WO2025037271A1
Provided herein are methods and assays for detecting central nervous system (CNS)-derived tau peptides in blood-based samples from subjects, involving the use of a capture antibody that binds to a tau epitope, and a detection antibody that binds to an epitope comprising amino acids residues that span the junction of Exon 4 and Exon 5 of CNS-derived tau.