Resumen de: WO2021222025A1

The present invention relates to IL-34 antibodies, compositions comprising the same, and methods of using the antibodies and or compositions thereof for treating immune-mediated diseases such as neurodegenerative diseases, for example Alzheimer's Disease or a tauopathy disease.

Resumen de: WO2021222263A2

Compositions and methods for detecting components of the inflammasome in a sample from a subject as markers for inflammasome-related diseases or disorders such as multiple sclerosis, stroke, mild cognitive impairment, Alzheimer's disease, age-related macular degeneration, NASH, inflammaging or traumatic brain injury. Methods of using such inflammasome markers to determine prognosis, direct treatment and monitor response to treatment for the subject with an inflammasome-related disease or disorder such as multiple sclerosis, stroke, mild cognitive impairment, Alzheimer's disease, age-related macular degeneration, NASH, inflammaging or traumatic brain injury are also described.

Resumen de: AU2017408873A1

A method for identifying pre-disposition to cognitive decline in a subject, the method comprising determining levels of: (a) omega-3 fatty acids, and vitamin D or a metabolite thereof; (b) omega-3 fatty acids, and homocysteine; (c) vitamin D or a metabolite thereof, and homocysteine; or (d) omega-3 fatty acids, vitamin D or a metabolite thereof, and homocysteine, independently in one or more samples obtained from the subject.

Resumen de: US2023067811A1

In some embodiments herein, methods, compositions, and uses for modulating lymphatic vessels of the central nervous system are described. In some embodiments, methods, compositions, or uses for treating, preventing, or ameliorating symptoms of a neurological disease comprise increasing flow via meningeal lymphatic vessels are described.

Resumen de: AU2021303517A1

The present invention provides a system for the study of tau protein aggregation in neuronal cells in vitro which can be used to screen agents for therapeutic effectiveness against aggregates of tau protein or fragments thereof.

Resumen de: US2023063416A1

A polytherapy of orally available compounds is disclosed that synergistically modulates and induces the expression of the cathelicidin gene (CAMP), which encodes the host defense peptide LL-37. By providing a number of different CAMP-inducing compounds together at the same time, stronger gene induction is achieved than with just one or two compounds, because the mechanism of induction broadens. Induction also may vary in different pas of the body depending on which compounds are used, and at what levels. We show for the first time that the polytherapy can induce cathelicidin expression in the brain, which may help to treat or prevent Alzheimer's Disease Systemic cathelicidin gene induction may help treat numerous other conditions including Type 2 Diabetes/Metabolic Syndrome, or chronic bacterial, viral, or fungal infections associated with increased cancer risk or neurodegeneration. By increasing cellular autophagy and macroautophagy and supporting mitochondrial biogenesis and homeostasis, CAMP gene upregulation may reduce the effects of cellular aging and increase longevity.

Resumen de: AU2021317020A1

The present invention refers to p53 sequence and post translational modifications (PTMs) and to their use as biomarkers in the diagnosis of neurodegenerative disease and cognitive decline and/or in the prognosis of Alzheimer's disease at different stages and/or of neurodegenerative disease in a biological sample. The invention also provides for a 1) diagnostic method based on a highly accurate mass spectrometry analysis for the diagnosis of neurodegenerative disease, including Mild Cognitive Impairment (MCI), Alzheimer's disease (AD), fronto-temporal dementia (FTD), Lewi's Body (LB), and vascular dementia (VD) in a subject, by evaluating the PTMs to the said p53 linear sequence protein and possible cut of its full sequence specifically in human plasma of patients; and 2) prognosis of AD in CU and MCI patients.

Resumen de: US2023054852A1

The present invention refers to p53 sequence and post translational modifications (PTMs) and to their use as biomarkers in the diagnosis of neurodegenerative disease and cognitive decline and/or in the prognosis of Alzheimer's disease at different stages and/or of neurodegenerative disease in a biological sample. The invention also provides for a 1) diagnostic method based on a highly accurate mass spectrometry analysis for the diagnosis of neurodegenerative disease, including Mild Cognitive Impairment (MCI), Alzheimer's disease (AD), fronto-temporal dementia (FTD), Lewi's Body (LB), and vascular dementia (VD) in a subject, by evaluating the PTMs to the said p53 linear sequence protein and possible cut of its full sequence specifically in human plasma of patients; and 2) prognosis of AD in CU and MCI patients.

Resumen de: US2023054073A1

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 CD163, 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: AU2021313706A1

Analysis of microRNA (miRNA) signatures to determine or predict stages of cognitive impairment and likelihood of Alzheimer's disease in an individual.

Resumen de: WO2023020664A1

The invention relates to a peptide, comprising an amino acid sequence selected from the group consisting of SEQ ID NO: 1, or SEQ ID NO. 2, SEQ ID NO: 3, SEQ ID NO: 4, SEQ ID NO: 5, SEQ ID NO: 6 or SEQ ID NO: 7, homologs, fragments and parts thereof, to a peptide of this type for the treatment of Alzheimer's disease and to the use of a peptide of this type for the identification, quantitative and/or qualitative determination of amyloid-ß fibrils, amyloid-ß oligomers and/or amyloid-ß aggregates.

Resumen de: WO2021195750A1

The present invention provides a method of treating or delaying the onset of Alzheimer's disease or other neurological diseases in a patient having or at risk of developing Alzheimer's disease or other neurological diseases comprising administering to the subject an effective amount of an anti-angiogenic agent. In particular, the present invention provides a method of treating and/or delaying the onset of Alzheimer's disease or other neurological diseases by inhibiting Angiopoietin-2 mediated Tie-2 angiogenic pathway comprising administering to the subject an effective amount of an inhibitor of the Angiopoietin-2 mediated Tie-2 angiogenic pathway.

Resumen de: WO2018221212A1

The present invention addresses the problem of providing a marker and an application thereof useful for early diagnosis or differentiation of Alzheimer's disease. Provided is a biomarker for Alzheimer's disease, comprising a blood-borne flotillin.

Resumen de: US2023047178A1

Described herein are compounds of formula (I), and pharmaceutically acceptable salts, solvates, hydrates, isotopically labeled derivatives and radiolabeled derivative thereof, and pharmaceutical compositions thereof. Also provided are methods and kits involving the inventive compounds or compositions for detecting and imaging Tau aggregates in the brain for detection of Alzheimer's disease (AD) in a subject.

Resumen de: US2023047413A1

Monoclonal anti-PHF-tau antibodies and antigen-binding fragments thereof are described. Also described are nucleic acids encoding the antibodies, compositions comprising the antibodies, methods of producing the antibodies, and use of the antibodies for treating or preventing conditions such as tauopathies.

Resumen de: KR20230021958A

본 발명은 GPR 4를 포함하는 신경퇴행성 질환 진단용 바이오 마커에 관한 것으로, 보다 상세하게는 신경 독소로 자극된 신경 세포에서 GPR4의 발현이 증가하는 것을 확인하여, GPR4의 발현량에 따라 신경퇴행성 질환 여부를 진단하고 이의 길항제를 이용한 신경퇴행성 질환을 치료하는 방법을 제공한다.

Resumen de: WO2023012064A1

The present invention relates to a method for identifying whether a mammal suffers from or is likely to suffer from Alzheimer's disease (AD) and/or a mild cognitive impairment (MCI), using a phenotypic signature as generated using multivariate classification algorithms. Moreover, the present invention relates to a method for stratifying a mammal into a healthy group or a group suffering or likely to suffer from Alzheimer's disease (AD) and/or a mild cognitive impairment (MCI) for a treatment against said disease. In addition, the present invention relates to a method for monitoring the progression of Alzheimer's disease (AD) and/or mild cognitive impairment (MCI) and/or the treatment state thereof in a mammal being treated against said Alzheimer's disease (AD) and/or mild cognitive impairment (MCI). The present invention also relates to a marker panel for identifying whether a mammal suffers from or is likely to suffer from Alzheimer's disease (AD) and/or a mild cognitive impairment (MCI), comprising PBMC-markers as identified. Furthermore, the present invention relates to a use of said marker panel and/or phenotypic signature for diagnostic and/or drug de-risking applications.

Resumen de: WO2021083977A1

The present invention relates to a molecular signature of the silent phase of Alzheimer's disease; and to methods using the same, for diagnosing a silent stage of Alzheimer's disease in a subject, stratifying a silent phase of Alzheimer's disease in a subject into different grades of the silent phase, prognosticating the progress of a silent phase of Alzheimer's disease in a subject, and determining a personalized course of treatment in a subject affected with a silent phase of Alzheimer's disease. It also relates to a computer system comprising a machine learning algorithm trained for diagnosing a silent phase of Alzheimer's disease in a subject.

Resumen de: WO2021195431A1

The present disclosure provides treatments for neurodegenerative disorders and more particularly to methods for treatment of patients with Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), or Alzheimer's disease of different degrees of severity. The methods for treatment of patients who have suffered neurodegenerative diseases and specifically MS, ALS, or Alzheimer's disease includes administering a xenon gas mixture in subjects with elevated levels of neurodegenerative microglia (MGnD), e.g., determined based on levels of inflammatory biomarkers, measured in blood, serum and CSF, or levels of CLEC7A (Dectin-1)/Translocator Protein (TSPO) expression, e.g., measured using TSPO imaging.

Resumen de: WO2021195750A1

The present invention provides a method of treating or delaying the onset of Alzheimer's disease or other neurological diseases in a patient having or at risk of developing Alzheimer's disease or other neurological diseases comprising administering to the subject an effective amount of an anti-angiogenic agent. In particular, the present invention provides a method of treating and/or delaying the onset of Alzheimer's disease or other neurological diseases by inhibiting Angiopoietin-2 mediated Tie-2 angiogenic pathway comprising administering to the subject an effective amount of an inhibitor of the Angiopoietin-2 mediated Tie-2 angiogenic pathway.

Resumen de: WO2019098763A2

The present invention relates to anti-α-synuclein antibodies, which preferentially recognize α-synuclein aggregates, and uses for detection, diagnosis, and/or treatment or prevention of a variety of diseases or disease symptoms related thereto due to accumulation of α-synuclein aggregates by using the anti-α-synuclein antibodies.

Resumen de: CN115698721A

The present invention relates to a method for assisting in the prediction of stroke and/or dementia in a subject comprising a) determining the amount of biomarker RET (transfection rearrangement) in a sample from the subject, b) comparing the amount determined in step a) to a reference, and c) assisting in the prediction of stroke and/or dementia. The invention further relates to a method for assisting in the assessment of the extent of white matter lesion in a subject, a method for assisting in the assessment of whether a subject has experienced one or more asymptomatic strokes, and a method for assisting in the diagnosis of atrial fibrillation in a subject. The invention further encompasses corresponding uses.

Resumen de: AU2022283622A1

Abstract Disclosed herein are methods and compositions for identifying and/or treating subjects having or likely to have amyotrophic lateral sclerosis (ALS) or frontotemporal dementia (FTD). Antibodies specific for one or more di-amino acid repeat-containing proteins are also provided herein.

Resumen de: US2023032690A1

The invention relates to the identification of a new Tau species starting at residue Met11 (Met11-Tau) which is N-alpha-terminally acetylated form (N-alpha-acetyl-Met11-Tau species: Ac-Met11-Tau). Several monoclonal antibodies specific of this new Tau species have been developed. One of this antibody, 2H2/D11, was used in THY-Tau22 mouse model (that develops with age neurofibrillary degeneration (NFD) and memory deficits), and N-alpha-Ac-Met11-Tau species were clearly detected early in neurons displaying NFD on hippocampal brain sections while it is not reactive in hippocampus from elderly controls. Finally, by using ELISA sandwich specific of Ac-Met11-Tau species, Alzheimer Disease (AD) brain samples are clearly discriminated from human elderly control brains. Thus the invention relates to this new Tau species starting from the methionine residue at position 11 said methionine being N-alpha acetylated. The invention also relates to antibody that specifically binds this new tau species, a method of detection of this new Tau species and a method of diagnosis of Tauopathy disorder.

Resumen de: US2023033235A1

The NXNL2 gene encodes by alternative splicing for a trophic factor RdCVF2 that enhances the function and the survival of neurons involved in long term memory. Now the inventors demonstrated that the cell surface receptor for the trophic factor RdCVF2 is NPTN65. The set-up of methods that could be used to screen for small molecules, agonists of RdCVF2 signaling in the brain would be suitable for the development of a future metabolic and redox treatment of tauopathies and in particular Alzheimer's disease.