University of South Florida

The United States Government As Represented by the Department of Veterans Affairs

Meganano Biotech, Inc.

Chuanhai Cao

Jianfeng Cai

Xiaoyang Lin

Jun Tan

Gary W Arendash

Haifan Wu

Yaqiong Li

Ge Bai

Huntington Potter

Kenneth E Ugen

Steven Specter

Susan B Nyland

Disclosed herein are exogenous antigen sensitized immature dendritic cells. The dendritic cell may also be dead. The exogenous antigen sensitized immature dendritic cells may be used to elicit an increased immune response. Further provided are vaccines comprising the exogenous antigen sensitized immature dendritic cells, methods, of inducing an immune response in a patient, and methods of treating a disease.

Dead antigen stimulated immature heterogenous dendritic cells as therapeutics for diseases

Provided herein are compounds, compositions, pharmaceutical compositions, kits, and methods relating to novel sulfono-γ-AA peptides. Novel sulfono-γ-AA peptides as described herein can have the structure according to Formula 1: In embodiments according to the present disclosure, novel sulfono-γ-AA peptides as described herein have minimal toxicity, can repair neuronal damage, inhibit Amyloid beta aggregation, and promote cellular growth and viability.

Compositions and methods relating to novel sulfono-gamma-AA peptides

Alzheimer's disease is treated using THC (alone, or in combination with melatonin) administered in an ultra-low dose amount sufficient to (i) reduce A&#x3b2; protein levels; (ii) reduce A&#x3b2; aggregation: (iii) maintain A&#x3b2;PP protein levels; (iv) enhance mitochondrial functioning; (v) decrease phosphorylation of GSK-3&#x3b2; protein; (vi) decrease GSK-3&#x3b2; protein levels; (vii) decrease phosphorylation of Tau protein; and/or (viii) maintain Tau protein levels, in said patient without severe psychological impairments and side effects associated with higher doses of THC.

Extreme low dose THC as a therapeutic and prophylactic agent for Alzheimer's disease

Disclosed herein are compounds for the treatment of neurodegenerative diseases and compositions comprising the same.

Compounds and methods for reducing or inhibiting aggregation of proteins in a subject

Alzheimer's disease is treated using THC (alone, or in combination with melatonin) administered in an ultra-low dose amount sufficient to (i) reduce A&#xdf; expression; (ii) reduce A&#xdf; aggregation: (iii) maintain APP expression; (iv) enhance mitochondrial functioning; (v) decrease phosphorylation of GSK3&#xdf; protein; (vi) decrease the expression of GSK3&#xdf; protein; (vii) decrease phosphorylation of Tau protein; and/or (viii) maintain Tau protein expression, in said patient without severe psychological impairments and side effects associated with higher doses of THC.

Ultra-low dose THC as a potential therapeutic and prophylactic agent for Alzheimer's disease

Compounds for the treatment of neurodegenerative diseases

The present invention pertains to a dendritic cell-based vaccine against rh-&#x3b1;-Syn, &#x3b1;-synuclein specific peptide antibodies and related vaccines, and methods of treating, inhibiting, and/or vaccinating against Parkinson's Disease (PD), or symptoms thereof.

Methods, antibodies, and vaccines utilizing epitopes of alpha synuclein for treatment of Parkinson's disease

The present invention pertains to a dendritic cell-based vaccine against rh-&#x3b1;-Syn, &#x3b1;-synuclein specific peptide antibodies and related vaccines, and methods of treating, preventing, and/or vaccinating against Parkinson's Disease (PD), or symptoms thereof.

Methods, antibodies, and vaccines utilizing epitopes of alpha synuclein for treatment of parkinsons disease

A method of treating and preventing a neurological disorder, such as Alzheimer's disease, in a subject in need thereof by positioning an electromagnetic field emitting source proximal to the subject and exposing the subject to an electromagnetic field having a predetermined frequency (preferably &#x2248;300-3,000 MHz) for a predetermined absorption period (preferably greater than &#x2248;3 days). Each individual treatment (comprising exposure to the predetermined frequency for the predetermined absorption period) is continued at a predetermined schedule for a predetermined treatment period. The EMF can have a specific absorption rate up to about 8 W/kg. The methodology enhances cognition in the subject and/or treats/prevents the underlying neurological disorder or a symptom thereof.

Prevention and treatment of brain diseases and disorders related to abnormal protein aggregation through electromagnetic field treatment

Embodiments of the present disclosure provide for &#x3b3;-AApeptides, &#x3b3;-AApeptide building blocks, methods of making &#x3b3;-AApeptides and libraries of &#x3b3;-AApeptides, methods of screening the &#x3b3;-AApeptide libraries for desired peptidomimetic activity, and the like. The present disclosure also provides for &#x3b3;-AApeptides that are inhibitors of A&#x3b2; peptide aggregation, methods of inhibiting and disassembling A&#x3b2; peptide aggregation, methods of inhibiting the toxicity of A&#x3b2; aggregates towards N2a neuroblasotma cells, as well as methods and compounds for treating Alzheimer's disease.

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The invention includes a method of treating and preventing a neurological disorder, such as Alzheimer's Disease, in a subject in need thereof by positioning an electromagnetic field emitting source proximal to the subject and exposing the subject to an electromagnetic field having a predetermined frequency for a predetermined absorption period. Preferably, each individual treatment (comprising exposure to the predetermined frequency for the predetermined absorption period) is continued at a predetermined schedule (preferably daily) for a predetermined treatment period. The predetermined frequency, according to a preferred embodiment, is about 918 MHz with a specific absorption rate (SAR) of about 0.25 W/kg+/&#x2212;2 dB. The predetermined absorption period of this preferred embodiment is about one hour. The treatment period is long-term, being greater than about 6 months and preferably between about 7 and 9 months.

Prevention and treatment of alzheimer'S disease through electromagnetic field exposure

Changes in adaptive immune system were identified and correlated as a predictor of A&#x3b2;and A&#x3b2;and AD progression. T-cell, B-cell, TCR and BCR profiles were used to correlate clinical progression of AD. The CDR3 region was spectratyped, showing the clonality of the CDR3 region. This intrafamily gene fragment length profile was compared to age-matched controls, thereby indicating the existence of a neurodegenerative disease. The novel method is useful in diagnosing neurodegenerative disease, like Parkinson's disease, HIV-associated Dementia, or Alzheimer's disease. Moreover, this permits the clinical identification of patients at a very early stage of AD and/or monitoring the potential benefits of disease modifying therapeutics.

Method of diagnosing or assessing risk for Parkinson's disease or Alzheimer's disease using TCR clonality

The application describes several mutant amyloid beta peptides and specific regions which are useful in the therapeutic and diagnostic of neurological diseases. The application further describes methods of using these mutant peptides as treatment and reagents for diagnosis of diseases. The application further describes diagnostic kits and pharmaceutical compositions for use in therapy to treat neurological diseases including but not limited to Alzheimer's disease and various forms of mild cognitive impairments.

Growing community of inventors

Tampa, FL, United States of America

Chuanhai Cao