Neurodegenerative disorders
Inventors
GREENFIELD, SUSAN ADELE • POTTIEZ, Gwenael • GARCIA-RATES, Sara Esther
Assignees
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Publication Number
US-10729749-B2
Publication Date
2020-08-04
Expiration Date
Abstract
The invention relates to novel peptides, compositions, therapies and methods for treating neurodegenerative disorders, for example Alzheimer's disease.
Core Innovation
The invention relates to methods for reversing or decreasing toxicity induced by T30 or amyloid beta to cell viability. The described approach contacts a cell with an effective amount of one or more peptides defined by specific amino acid sequences set out in SEQ ID No: 30, 32, 40, 42, 48, 51 or 53.
The description links the neurodegenerative mechanism to AChE/catalytic-independent peptides derived from tailed acetylcholinesterase, aberrantly activated development, and trophic-toxic effects in relation to global neurons. The toxic effects are described as being mediated by an induction of calcium influx and toxicity that can be synergistic with amyloid beta.
The invention further associates the protective action of the peptides with decreasing calcium influx and increasing acetylcholinesterase activity. It presents specific small linear peptides derived from the C-terminus of tailed acetylcholinesterase in the context of T30 and/or amyloid beta challenge, including a strategy in which protective peptides for T30 toxicity are used together with protective peptides for amyloid beta toxicity.
Claims Coverage
The independent claim covers a method for reversing T30- or amyloid beta-induced toxicity to cell viability using one or more peptides with amino acid sequences defined by SEQ ID No: 30, 32, 40, 42, 48, 51 or 53. Six inventive features are reflected across the claim set, with dependent claims refining peptide selection, number of peptides, and combination use.
Reversing T30 or amyloid beta induced toxicity to cell viability
A method comprising contacting a cell with an effective amount of one or more peptides to reverse T30 or amyloid beta induced toxicity to cell viability.
Decreasing calcium influx
The method results in decreasing calcium influx as part of reversing T30 or amyloid beta induced toxicity.
Increasing acetylcholinesterase activity
The method results in increasing acetylcholinesterase activity as part of reversing T30 or amyloid beta induced toxicity.
Using specific SEQ ID No peptides (30, 32, 40, 42, 48, 51 or 53)
The contacting is with one or more peptides consisting of an amino acid sequence as set out in SEQ ID No: 30, 32, 40, 42, 48, 51 or 53.
Contacting more than one peptide
The method further comprises contacting a cell with an effective amount of more than one peptide.
Protective combination for both T30 and amyloid beta toxicity
The method includes contacting using protective peptides against T30 toxicity together with protective peptides against amyloid beta toxicity in combination.
Overall, the claim coverage centers on contacting cells with effective amounts of specific SEQ ID-defined linear peptides to reverse T30 or amyloid beta induced toxicity to cell viability, characterized by decreasing calcium influx and increasing acetylcholinesterase activity. Dependent claims refine the choice of which SEQ ID peptide(s) are used, allow more than one peptide, and specify combination use that can include protection against both T30 and amyloid beta toxicity.
Stated Advantages
Reverses T30 or amyloid beta induced toxicity to cell viability.
Decreases calcium influx.
Increases acetylcholinesterase activity.
Documented Applications
No documented applications found
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