Resumen de: CN116064763A
The invention relates to the field of disease diagnosis and treatment, in particular to disease diagnosis and treatment with IFP35 and NMI as targets. The invention discloses application of interferon-induced protein 35kD and/or detection of N-Myc interaction protein in diagnosis or prognosis evaluation of inflammatory bowel diseases, arthritis, psoriasis, systemic lupus erythematosus, nervous system diseases, lung injury and peritonitis, in evaluation of the severity of arthritis and in distinguishing of tumor diseases and thoracic infection diseases for the first time. The ROC curve chart shows that the interferon-induced protein 35kD and/or the N-Myc interaction detection protein can be used as a marker for diagnosis or prognosis evaluation of inflammatory bowel diseases, arthritis, psoriasis, systemic lupus erythematosus, nervous system diseases, lung injury and peritonitis, evaluation of the severity of arthritis and distinguishing of tumor diseases and thoracic infection diseases.
Resumen de: WO2024177086A1
Provided is a method for evaluating dementia risk, the method allows direct understanding of the physical state of a subject through an analysis of a biological sample of the subject, and objective and highly accurate evaluation of the risk of the subject who might be developing dementia (mild cognitive impairment (MCI) or Alzheimer's disease (AD)). Concentration data regarding an element group for evaluation in a blood (plasma or serum) sample 2 taken from a subject are acquired (step S1), the concentration data are applied to a discriminant function that determines whether the subject belongs to a control group or a case group, and a correlation between concentrations of the group of elements for evaluation is calculated (step S2), and on the basis of the correlation, an indicator as to whether the subject is suffering from dementia is obtained (step S3). As the group of elements for evaluation, a combination of the 17 elements Na, Mg, P, S, K, Ca, Fe, Co, Cu, Zn, As, Se, Rb, Sr, Mo, Ag, and Cs is used. It is preferable that an estimation that the type of dementia that the subject is suffering from is MCI or AD is included in evaluation results.
Resumen de: US2024285727A1
Described herein is a novel, mitochondrial encoded, open reading frame that leads to the production of a new mitochondrial peptide called SHMOOSE. SHMOOSE is a 58-amino-acid peptide and, within its open reading frame, contains a genome-wide significant small nucleotide polymorphism (SNP) that markedly increased risk for Alzheimer's disease, brain structure, brain gene expression, and cognition. SHMOOSE increased neuronal-type cell survival and protected against amyloid beta toxicity. Metabolomic studies revealed a role for the peptide in energy optimization, whose dysfunction and dysregulation leads to cell death in physiologically notable regions of the brain in neurodegenerative diseases such as Alzheimer's and Parkinson's. Methods and compositions, including peptide analogues and derivatives, are described for treatment and diagnostics.
Resumen de: US2024287471A1
The disclosure relates to compositions and methods for treatment of diseases associated with aberrant lysosomal function, such as fronto-temporal dementia (FTD). The disclosure also provides expression constructs comprising a transgene encoding progranulin or a portion thereof. The disclosure provides methods of treating FTD by administering such expression constructs to a subject in need thereof.
Resumen de: AU2022354161A1
The invention relates to skin biomarkers, and in particular, to skin biomarkers for diagnosing and prognosing neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, as well as diagnostic and prognostic methods and kits for these conditions. The invention also provides methods of treating neurodegenerative disorders. The invention further provides the use of biomarkers in the skin for skin aging (biological & chronological), and kits for detecting and quantifying skin aging, and also methods for treating, preventing or slowing down skin aging.
Resumen de: US2024280591A1
A method for detecting p217+tau in blood-based samples from a subject with high sensitivity, accuracy, and precision. The assay comprises contacting a sample with a capture antibody directed against a p217+tau epitope to bind the capture antibody to p217+tau peptides in plasma to form antibody-peptide complexes, and separately contacting the antibody-peptide complexes with a detection antibody to bind the detection antibody to the antibody-peptide complexes. The amount of p217+tau is determined by detecting the detection antibody. The amount of p217+tau detected is used to determine whether the subject has tauopathy or is at risk of developing tauopathy, or whether the subject has amyloidogenic disease or is at risk of developing amyloidogenic disease when the amount of p217+tau peptides is above a predetermined threshold value. The method has improved sensitivity such that the predetermined threshold value is above a Lower Limit of Quantification and/or Lower Limit of Detection of the assay.
Resumen de: US2024280566A1
The present disclosure provides a system comprising a communication interface and computer for assigning a label to the biomolecule fingerprint, wherein the label corresponds to a biological state. The present disclosure also provides a sensor arrays for detecting biomolecules and methods of use. In some embodiments, the sensor arrays are capable of determining a disease state in a subject.
Resumen de: EP4273882A2
Provided herein are methods of developing pharmaceuticals for treatment of neurodegenerative conditions, such as synucleopathic conditions, amyloidopathic conditions, tauopathic conditions, and Huntington's disease. The methods involve using a biomarker to determine the effect of a candidate pharmaceutical on the condition. The biomarker profile includes quantitative measures of each of one or a plurality of neurodegenerative protein forms, wherein the neurodegenerative proteins are, e.g., alpha-synuclein and, amyloid beta, tau or huntingtin. Biomarker profiles include one or more oligomeric forms and, optionally, one or more monomeric forms of the neurodegenerative protein. Neurodegenerative proteins can be quantified from, e.g., CNS-derived exosomes from the blood of a subject.
Resumen de: US2024270843A1
The present invention provides a method of treating a condition or disorder associated with microglial dysfunction in a human patient, such as Alzheimer's disease, comprising administering to the patient a TREM2 agonist. In another aspect, the invention provides a method of assaying a biological sample taken from a patient having such a condition, such as Alzheimer's disease, for biomarkers characteristic of microglia activity in order to determine treatment benefit or whether the disease has an increased probability of responding to treatment with a TREM2 agonist.
Resumen de: AU2022439338A1
Disclosed herein are methods of diagnosing, selecting, monitoring, and treating subjects with Alzheimer's disease (AD) or suspected of having AD or another disorder associated with amyloid accumulation in the brain.
Resumen de: AU2023207441A1
The invention relates to an
Resumen de: WO2023057875A1
Method for the early diagnosis and the monitoring of the evolution/regression of neurodegenerative pathologies, said method providing for the quantification of a. biomarker for said pathologies in a fluid that was previously drawn from a. patient, said fluid being selected from among: cerebrospinal fluid; serum; urine; post mortem cerebral tissues and cellular lysates, said method being characterized in that the quantified biomarker is selected from among native proNGF; modified proNGF, the latter being proNGF in its forms with higher molecular weight, including forms of 39-40 kDa and 45-50kDa; NGF; and the proNGF/NGF ratio, said method sequentially providing for the fol lowing steps of Preparation of the biological sample, Definition of the calibration curve; Execution of run and interpolation.
Resumen de: AU2022408967A1
Described herein are improvements relating to IGF-1 function analysis, adjustment and its application in disease management of non-neurological and/or neurological conditions. More specifically, methods relating to the clinical application of cyclic glycine-proline (cGP) and/or cGP/IGF-1 molar ratio as the plasma biomarker for prediction of risk and recovery of non-neurological and/or neurological conditions with IGF-1 dysfunction and the use of a cGP containing animal, marine or fungal based material such as concentrate/extract of hydrolysed bovine collagen and marine collagen, mushroom and seaweed along with plant-based cGPMAX™ for the treatment of same. The methods more accurately measure IGF-1 function in vivo indirectly using cGP and cGP/IGF-1 molar ratio along with a means to adjust and normalise cGP and cGP/IGF-1 molar ratio (and hence active IGF-1 concentration), and specific treatment methods for individuals with a lower or reduction of cGP level relative to a standard set of baseline data. Supplementation of bovine collagen formulated cGPMAXTM effectively improved the sensory function in patients with diabetic neuropathy.
Resumen de: WO2024161163A2
Declining cerebral blood flow leads to chronic cerebral hypoperfusion which can induce neurodegenerative disorders, such as vascular dementia. The reduced energy supply of the brain impairs mitochondrial functions that could trigger further damaging cellular processes. Altered levels of protein biomarkers are discloses to be useful in the diagnosis of vascular dementia.
Resumen de: WO2024163454A1
Synucleinopathies are a group of neurodegenerative diseases including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). These diseases are characterized by the aggregation and deposition of α-synuclein (α-syn) in Lewy bodies (LBs) in PD and DLB or as glial cytoplasmic inclusions in MSA. In healthy brains, only ~4 % of α-syn is phosphorylated at Ser129 (pS129-α-syn), whereas > 90% pS129-α-syn may be found in LBs. Embodiments of the invention include a duplex assay for both total α-synuclein and pS129-α-synuclein, which allows measuring both analytes in the same sample, leading to substantial saving in sample volume. The assays can be widely used in methods for detecting pS129-α-syn in biomedical studies including when only a limited volume of sample is available and high sensitivity is required, offering new opportunities for diagnostic biomarkers, monitoring disease progression, and quantifying outcome measures in clinical trials.
Resumen de: WO2023128904A1
The current invention is related to detecting risk biomarkers for chronic neurodegenerative disorder of central nervous system called Alzheimer's disease (AD). AD is the most common cause of dementia, and it is characterized by extracellular senile plaques formed by the accumulation of amyloid β (Aβ) proteins and aggregation of tau proteins into intracellular neurofibrillary tangles in central nervous system. The present invention aims at developing a novel PoC based multiple AD biomarkers detection assay and method, such as Aβ1- 40/Aβ1-42, tau protein and BDNF using multi-colored highly luminescent, non-photo-bleaching quantum dots (QDs), which provides an affordable and accurate means for early diagnosis of MCI, AD or dementia at homes, hospitals or near the patient bedsides.
Resumen de: CN117980322A
The present invention relates to biomarker panels and methods for their use in the diagnosis, staging, treatment and assessment of therapeutic response to neurocognitive disorders characterized by tau toxicity, such as Alzheimer's disease. Comprising phosphorylated peptides at at least three positions, and can be used as biomarkers for screening neurocognitive impairment.
Resumen de: KR20240118211A
본 발명은 TIMP-3 단백질 및/또는 이를 암호화하는 유전자를 포함하는 경도인지장애 또는 알츠하이머성 치매의 진단용 조성물 및 이를 이용한 진단용 정보제공방법에 관한 것으로, 보다 구체적으로는 경도인지장애 또는 알츠하이머성 치매 환자군의 혈장 및 뇌척수액에서 TIMP-3 단백질의 발현이 정상대조군에 비해 유의하게 낮아 이를 경도인지장애 또는 알츠하이머성 치매의 진단에 이용할 수 있음을 확인하여 발명으로 완성한 것이다.
Resumen de: US2024255530A1
Provided are methods of diagnosis and differentiation of and between PD and DLB tissue samples.
Resumen de: US2024255509A1
Provided herein are H1.0K180me2 antibodies, H1.0K180me2 proteins, and H1.0K180me2 peptides and methods of use for diagnostics and therapeutics. These H1.0K180me2 antibodies, H1.0K180me2 proteins, and H1.0K180me2 peptides may be used in the treatment of methylated H1.0-related diseases or conditions in an individual. These H1.0K180me2 antibodies, H1.0K180me2 proteins, and H1.0K180me2 peptides may also be used for the detection and quantification of a histone H1.0 protein or fragment thereof, comprising a dimethylated lysine at lysine residue 180 (H1.0K180me2); such compositions and methods are useful for detecting replicative senescence, DNA damage, genotoxic stress, radiation exposure, Alzheimer's disease, are useful for monitoring therapeutic regimens, patient stratification, drug screening, and may serve as a marker of biological aging in a system.
Resumen de: AU2023216231A1
Disclosed are methods for using regional tau PET scans for identifying a subject having or suspected of having, diagnosing, and treating Alzheimer's disease. The methods are particularly useful for treating and diagnosing a patient as susceptible and at risk for developing amyloid-beta and cognitive dysfunction using tau-PET imaging based on regional tau PET measures.
Resumen de: MX2024001835A
Compositions and kits for diagnosing and prognosing Alzheimer's Disease (AD) in a human patient include a binding agent such as a monoclonal antibody for a biomarker conjugated to a detectable moiety such as a fluorophore, wherein the biomarker is chosen from CD 163, CD91, CD59, MerTK and other phagocytosis-related molecules. Further compositions and kits employ panels of fluorophore-conjugated monoclonal antibodies for biomarkers including scavenger receptors. Methods for determining the relative expression of biomarkers, diagnosing AD, and determining the efficacy of AD therapeutic candidates such as phagocytosis-promoting agents and scavenger receptor agonists also appear.
Resumen de: CN118043671A
Methods of determining the presence of Alzheimer's disease (AD) in a living human subject using a serum or plasma sample preparation from the living human subject are disclosed. In one aspect, the presence of about 90 kDa filament A (FLNA) polypeptide fragments in the sample preparation indicates that the sample donor is likely to suffer from AD. More preferably, the ratio of the amount of the about 90 kDa FLNA polypeptide fragment to the amount of the full-length (about 280 kDa) FLNA protein in the sample preparation is determined. The donor may suffer from AD if the ratio is from about 10 to about 2000, and may not suffer from AD if the ratio is from about 0.005 to about 5. Also contemplated are methods for determining the prognosis of a treatment in a living human subject inferred to have Alzheimer's disease (AD), systems and kits for performing said assays.
Resumen de: US2024248100A1
Methods and compositions useful in treating neurodegenerative disorders are based on septapeptides and extended forms thereof (or portions thereof) that exhibit chemokine activity with respect to microglial cell precursors.
Nº publicación: US2024247054A1 25/07/2024
Solicitante:
MABWELL THERAPEUTICS INC [US]
MABWELL THERAPEUTICS, INC
Resumen de: US2024247054A1
The present disclosure provides anti-amyloid β (Aβ) antibodies and antibody fragments that preferentially bind soluble amyloid Aβ protofibril/oligomer and trigger ADPC in microglial cells, anti-amyloid β (Aβ) antibodies and antibody fragments that reduce soluble amyloid Aβ protofibril/oligomer levels and insoluble amyloid Aβ plaque in brain tissue, and the use of anti-Aβ protofibril/oligomer antibodies and antibody fragments in therapy, prophylaxis, diagnosis, screening, and monitoring of conditions associated with Aβ protein aggregation, in particular Alzheimer's disease (AD).