17 results about "Atrophic spinal cord" patented technology

The present disclosure provides herein, inter alia, methods of treating patients diagnosed with amyotrophic lateral sclerosis (ALS).

Compositions and methods of using same for treating Amyotrophic Lateral Sclerosis (ALS) are provided. Accordingly there is provided a method of treating ALS in a human subject in need thereof, the method comprising intravenously (IV) administering to the subject 2 - 5 mg / kg of a peptide comprising an amino acid sequence as set forth in SEQ ID NO: 1. Also provided are compositions and unit dosage forms comprising a peptide comprising an amino acid sequence as set forth in SEQ ID NO: 1. 20 25 20 10 60 14 F eb 2 02 5 3 9 A B S T R A C T 2 0 2 5 2 0 1 0 6 0 1 4 F e b 2 0 2 5

The present invention relates to the treatment of an ALS patient with oral trimetazidine. This results in an anticipated 25-50% reduction in the average decline over at least three months as measured using the revised ALS Functional Rating Scale.

Provided herein is an anti-CD2 antibody or antigen binding fragment thereof for treating and / or preventing ALS in a subject in need thereof.

Abstract Dosage regimens for SOD1-targeting antisense oligonucleotides, and salts thereof, are provided. These dosage regimens find use in the treatment of subjects having or at risk of developing amyotrophic lateral sclerosis. Abstract 20 26 20 53 14 06 J ul 2 02 6 A b s t r a c t 2 0 2 6 2 0 5 3 1 4 0 6 J u l 2 0 2 6

The subject matter described here relates to methods, compositions, and vectors for treating Amyotrophic Lateral Sclerosis (ALS) in a subject in need thereof. In certain aspects, the method comprises administering to the subject a composition comprising adeno-associated viruses (AAVs), wherein the AAVs comprise a nucleic acid sequence comprising an enhancer sequence and encoding one or more transcription factors that control gene expression in nascent motor neurons, wherein the enhancer is capable of driving a motor-neuron specific expression of the one or more transcription factors and wherein the one or more transcription factors are expressed in motor neurons of the subject.

Provided herein is an anti-CD2 antibody or antigen binding fragment thereof for treating and / or preventing ALS in a subject in need thereof.

The disclosure provides a method of predicting the onset of clinical manifestations of amyotrophic lateral sclerosis (ALS) in a human, the method comprising (a) measuring phosphorylated neurofilament heavy chain (pNfH) and / or neurofilament light chain (NfL) levels in a subject, and (b) predicting the onset of ALS, wherein increased levels of pNfH and / or NfL signal the onset of clinical manifestations of ALS.

The present invention relates inter alia to methods for identifying a substance useful for the prevention or treatment of a disease, disorder, or condition associated with altered NLRX1 activity, and uses of said substances in the prevention or treatment of a disease, disorder, or condition associated with altered NLRX1 activity, for example in the prevention or treatment of Parkinson's disease or amyotrophic lateral sclerosis.

Described herein are neonatal cardiac mesenchymal progenitor cells, an nMPC secretome, or an nMPC exosome for treating Amyotrophic Lateral Sclerosis (ALS) in a subject. One or more doses of neonatal cardiac mesenchymal progenitor cells, an nMPC secretome, an nMPC exosome, an nMPC total secretome, or a combination thereof can be administered to the subject. Neonatal cardiac mesenchymal progenitor cells can be allogeneic. The subject may also be administered one or more combination therapies.

The present invention provides a formulation of metformin and glibenclamide for the prevention and / or treatment of neurodegenerative diseases, preferably chosen among Parkinson's disease, multiple system atrophy, amyotrophic lateral sclerosis, frontotemporal dementia, Lewy body dementia, Huntington's disease and Alzheimer's disease.

It relates to a method for the treatment of famyotrophic lateral sclerosis (ALS) by an oligonucleotide agent, comprising the step of administering the subject a treatment effective amount of the oligonucleotide agent, wherein the oligonucleotide agent comprises a double-stranded targeting oligonucleotide (siRNA) and a non-targeting single-stranded accessory oligonucleotide (ACO). The method can be used in the treatment of ALS with and without SOD1 mutation. It also provides a safety therapeutic window and an effective dosing regimen for the treatment of ALS using the oligonucleotide agent.

The present disclosure provides herein, inter alia, methods of treating patients diagnosed with amyotrophic lateral sclerosis (ALS).

The disclosure provides methods of treating neurodegenerative conditions, for example, amyotrophic lateral sclerosis, using a regimen of a chlorite salt, for example, sodium chlorite. The long-term survival of subjects receiving sodium chlorite and placebo are compared.

Compounds described herein may be used for the treatment of neurodegenerative diseases linked to protein misfolding, including prion diseases, Alzheimer's disease, Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), and also other neurodegenerative, degenerative, metabolic and ischemic conditions. Indeed, NAD metabolism impairment is also a critical feature in brain ischemia / reperfusion injury, Wallerian degeneration, kidney failure, multiple sclerosis, aging, and metabolic disorders such as diabetes mellitus. Therapies that elevate or stabilize NAD levels may thus have broad potential for treating many severely debilitating neurological and metabolic conditions. Evidence is provided herein with compounds from 8 lead series for NAD restoring properties and for therapeutic efficacy in cellular and / or animal models of prion disease, PD and ALS.

An application method of brucine for treating amyotrophic lateral sclerosis (ALS) is provided, relating to the field of biomedicines. It can delay a time of onset of ALS, prolong survival time of ALS patients, delay a weakening of limb extension ability, and improve limb grip strength.

The invention described herein provides eIF2B agonist (e.g., COMPOUND 1 ) and uses thereof for treatment of diseases, especially neurodegenerative diseases, including vanishing white matter (VWM), Huntington's disease (HD), Charcot Marie Tooth syndrome (CMT), and Amyotropic Lateral Sclerosis (ALS).