43 results about "Amyloid beta proteins" patented technology

The present invention provides compositions and methods for diagnosing Alzheimer's disease (AD). In particular, the present invention provides monoclonal antibodies that specifically bind to soluble, non-fibrillar oligomeric amyloid β protein assemblies proteolytically derived from the transmembrane amyloid precursor protein (APP) while not reacting with fibrillar amyloid β protein assemblies, monoclonal antibodies that specifically bind to fibrillar amyloid β protein assemblies that do not react with soluble, non-fibrillar oligomeric amyloid β protein assemblies, and methods of use of these compositions in the diagnosis of Alzheimer's disease, as well as methods to monitor treatment and/or disease progression of AD in patients.

The present invention provides assemblies of oligomeric amyloid beta protein and uses thereof.

The present invention is directed to pharmaceutical agents and compositions useful for the treatment and prevention of amyloid disease in a subject. The invention further relates to isolated antibodies that recognize a common conformational epitope of amyloidogenic proteins or peptides that are useful for the diagnosis, treatment, and prevention of amyloid disease.

The present invention pertains to the prevention, treatment and diagnosis of neurodegenerative diseases, in particular Alzheimer's disease, and other similar disease. More specifically to high affinity antibodies selective for amyloid beta protein (Aβ) in its protofibril conformation and of IgG class and IgG1 or IgG4 subclass or combinations thereof or mutations thereof, retaining high Fc receptor binding and low C1(CIq) binding, effective in clearance of Aβ protofibrils and with reduce risk of inflammation.

Antisense nucleic acids, compositions and methods are provided for modulating the expression of an amyloid beta protein (AβP) portion of the amyloid precursor protein (APP) coding sequence. The compositions comprise antisense nucleic acids targeted to nucleic acids encoding amyloid precursor protein. Methods of using these nucleic acids for modulation of amyloid precursor protein expression and for treatment of diseases and conditions associated with expression of the amyloid beta protein portion of the amyloid precursor protein are provided.

The present invention relates to a novel channel structure of human amyloid beta protein (AbP) in lipid membranes and a rapid, quantitative and specific assay for screening test compounds, such as drugs, ligands (natural or synthetic), proteins, peptides and small organic molecules for their ability to bind and block the membrane AbP channels. The invention further relates to screening and identifying therapeutically relevant compounds for treating Alzheimer's disease and other disorders.

There is provided a series of macrocyclic diaminopropanes of Formula (I) or a stereoisomer; or a pharmaceutically acceptable salt thereof,

wherein R₁, R₂, R₃, m, n, W, X, Y, Z and L as defined herein, their pharmaceutical compositions and methods of use. These novel compounds inhibit the processing of amyloid precursor protein (APP) by β-secretase and, more specifically, inhibit the production of Aβ-peptide. The present disclosure is directed to compounds useful in the treatment of neurological disorders related to β-amyloid production, such as Alzheimer's disease and other conditions affected by anti-amyloid activity.

The invention relates to a preparation method of difunctional copolymerized nanoparticle inhibitor and application thereof in inhibition and detoxification of amyloid beta protein aggregation. The preparation method includes: using a connection product GMA-IDA of iminodiacetic acid (IDA) and glycidyl methacrylate (GMA) as a monomer; subjecting the monomer to free radical copolymerization reaction with monomers like N-isopropylaccrylamide (NIPAm) and n-tertbutyl acrylamide (TBAm) to synthesize the difunctional nanoparticle inhibitor having metal chelation ability and protein aggregation inhibiting ability. Average particle diameter of difunctional copolymerized nanoparticles synthesized by the method is 80-120nm. Metal ion chelation capacity of the nanoparticles synthesized by the method is higher than 700umol/g, and the nanoparticles can chelate metal ions in environment and inhibit fibrosis aggregation of Abeta42 and are a potential new drug raw material for treating Alzheimer's disease.

The invention discloses a drug for targeted therapy of Alzheimer's disease (AD) and a preparation method thereof. The drug is a magnetic mesoporous silica/siBACE1 nanocomposite modified by PHI polypeptide; the PHI polypeptide refers to C-FRHMTEQ-C, the siBACE1 refers to BACE1_5, the nanocomposite is characterized by taking Fe3O4 nanocrystal as a core, taking magnetic mesoporous structure as a coat, loading siBACE1 in mesoporous, enveloping surface of the coat with PEI and then modifying by KALA peptide and PHI polypeptide. siBACE1 serves as an effective component of the drug, PHI polypeptide serves as a targeted head group and magnetic mesoporous silica nanoparticles modified by high-molecular polymer serves as a carrier; thus, neurons BACE-1 expression is prevented in a targeted form, production and deposition of amyloid beta-protein of AD focal areas are suppressed, and then the purpose of relieving symptom of AD is achieved. The preparation method of the drug is easy and feasible, raw materials for preparing the drug are easy to obtain, the preparation process has good repeatability, and the drug prepared has high biocompatibility.

The present invention discloses use of rhodiola root and spine date seed compound polysaccharide in preparation of anti neurodegenerative disease health food, the compound polysaccharide is a composition of rhodiola root polysaccharide and spine date seed polysaccharide, the compound polysaccharide is prepared from rhodiola root and /or spine date seed as raw materials by water extraction, concentration and alcohol precipitation process, the preparation method is simple, stable, efficient, and suitable for industrial production. By caenorhabditis elegans model experiment verification, the rhodiola root and spine date seed compound polysaccharide can effectively inhibit neurotoxicity of amyloid beta-protein and polyglutamine, the action mode is related with toxic protein aggregation inhibition, heat shock protein expression increase and reactive oxygen free radical level reduction, and neuroprotective effect can be shown.

The invention relates to a component containing extracts of ilex latifolia as active ingredients and used for preventing or curing an ischemic disease or a degenerative brain disease. In particular, extracts of ilex latifolia taking water, alcohol or a mixture of water and alcohol as a menstruum restrain the cerebral infarction and dropsy on a rat having the cerebral infarction, and restrain the memory impairment on a rat having neurotoxicity caused by being injected an amyloid beta protein(amyloid beta protein; A beta(25-35)), and according to the injection volume, the oxidative stress caused by hydrogen peroxide, the excitatory amino acid glutamic acid, the A beta(25-35) causing the neurotoxicity, the death of cortical brain nerve cells caused by hypoxidosis etc. can be restrained. Therefore, the extracts of ilex latifolia can be used as drug components for preventing or curing the ischemic disease or the degenerative brain disease or used as active ingredients of functional health food.

The invention belongs to the technical field of medicines, and discloses an application of needle-leaved polyprenol in preparing medicines for preventing and treating Alzheimer disease. The needle-leaved polyprenol is obtained from needle leaves of pinaceae plants such as pinus, picea, larch, fir and cedar and the like by extraction, separation and purification. The needle-leaved polyprenol is long-chain polyterpene compound formed by 14-24 isopentene group units. Cell and animal experimental results indicates that the needle-leaved polyprenol has functions of preventing and treating the Alzheimer disease, i.e., the needle-leaved polyprenol has a protection function for damage of pheochromocytoma (PC) 12 nerve cells caused by amyloid-beta protein, and can improve the passive avoidance memory capability and space learning memory capability of demented mice. Therefore, the needle-leaved polyprenol can be used for preparing the medicines for preventing and treating the Alzheimer disease.

The present invention discloses uses of butylidenephthalide, an analog thereof or a combination of the butylidenephthalide and the analog thereof in preparation of pharmaceutical compositions for treatment or prevention of neurodegenerative diseases, and a method for preparing the pharmaceutical composition from the butylidenephthalide. According to the present invention, the disclosed butylidenephthalide can reduce the intracellular amyloid beta-protein concentration so as to achieve the effect of treatment or prevention of neurodegenerative diseases; and according to the preparation method of the disclosed pharmaceutical composition, the polymer substance is adopted as the drug carrier to coat the butylidenephthalide adopted as the active component into the polymer substance so as to slow down or reduce the cytotoxicity of the butylidenephthalide, improve the safety of the pharmaceutical composition, and treat or prevent neurodegenerative diseases.

A compound represented by the following formula or a salt thereof:

wherein each of A¹, A², A³ and A⁴ independently represents a carbon or nitrogen; R¹ is a group selected from the group consisting of hydrogen, hydroxyl group, carboxyl group, sulfuric acid group, amino group, nitro group, cyano group, non-radioactive halogen substituents, alkyl substituents with 1-4 carbon atoms and alkoxy substituents with 1-4 carbon atoms; and R² is a radioactive halogen substituent, provided at least one of A¹, A², A³ and A⁴ represents a carbon, and R1 binds to a carbon represented by A¹, A², A³ or A⁴, is effective as an image diagnosis probe targeting amyloid and as well as a diagnostic agent for Alzheimer's disease including the compound represented by the above formula or a salt thereof.

The invention relates to a small molecule compound for inhibiting amyloid beta protein aggregation and a preparation method and application of the small molecule compound. The preparation method comprises the following steps: coupling glutamine by using carboxyl on the surface of 3,4,5-trihydroxybenzoic acid to obtain a 4-carbamoyl-2-[(3,4,5-trihydroxyphenyl)formylamino]butyric acid compound. The small molecule compound can effectively inhibit the aggregation of amyloid beta protein in a concentration range of 5-25 [mu] M, reduce the content of a beta folding structure and remove amyloid plaques in an Alzheimer's disease model caenorhabditis elegans CL2006 body, and the service life of the CL2006 is prolonged by one third. Compared with similar small-molecule and heterogeneous polypeptide or protein Alzheimer's disease inhibitors, the polypeptide or protein inhibitor has a remarkable amyloid protein inhibition effect and good blood-brain barrier penetrability; and the aggregation form of A[beta]42 can be changed, and the generation of amyloid protein fibers is inhibited. The compound has a wide application prospect in preparation of medicines for treating Alzheimer's disease.

This invention provides a convenient and industrially advantageous process producing amine derivatives having the action of inhibiting the secretion and accumulation of amyloid beta protein. In Compound (I), the ether linkage is selectively cleaved without cleaving the amide linkage present in the same molecule and tertiary amines are not converted into quaternary salts, and thus Amine Derivative (V) with good qualities having the action of inhibiting the secretion and accumulation of amyloid beta protein can be obtained in high yield.

The invention discloses application of plant extracts in drugs for preventing and treating senile dementia. The plant extracts comprise a fruit and vegetable extract containing fisetin and a fig juiceextract containing benzaldehyde, bergamot lipoid and psoralen. Senile dementia is believed to be associated with the deposition of amyloid beta protein and tau protein in the brain, and fisetin is asmall active molecule taken orally and can prevent memory loss associated with senile dementia. The fig juice extract containing benzaldehyde, bergamot lipoid and psoralen can make massive harmful proteins capable of causing dementia discharged from the brain and prevent the proteins from being accumulated in the brain. Accumulation of the massive harmful proteins capable of causing dementia in the brain is avoided, and the substances contained in the plant extracts have a significant inhibitory effect on triggering of dementia cells in the brain.