Galantamine clearance of amyloid ß
AssigneeSynaptec Development LLC
InventorBonnie M. DAVIS
Life of this patent
Estimating the term…
Abstract
Galantamine and its pharmaceutically acceptable salts are of use in treating persons meeting criteria for having a risk of developing Alzheimer's type dementia, before dementia occurs by reducing the decline of Aβ amyloid in CSF or the increase in cortical beta amyloid, in order to delay cognitive decline.
Claims30
A method for maintaining or increasing levels of Aβ42 in CSF. or reducing deposition of amyloid beta in cortex, in patients who are not demented, but who exhibit a decreased Aβ42 level in CSF or exhibit increased beta amyloid in cortex which comprises administering thereto a therapeutically acceptable, dose of galantamine or a pharmaceutically acceptable salt thereof, in order to delay cognitive or functional decline.
A method for maintaining or increasing levels of Aβ42 in CSF, slowing the deposition of beta amyloid in brain, clearing beta amyloid from brain, or slowing cognitive or functional decline of patients which comprises administering thereto a therapeutically acceptable dose of galantamine or a pharmaceutically acceptable salt thereof to a patient who has been assessed by one or more standard tests to have impaired cognition or function, or to have declining cognition or function, consisting of a 10% decline from baseline, or declines on three successive tests at least three months apart, but not to be displaying dementia, and not having a condition not associated with Alzheimer pathology to which the impaired cognition or function can be solely attributed, so as to delay deterioration of cognition and/or function.
17-18. (canceled)
A method for maintaining or increasing levels of Aβ42 in CSF of patients, reducing the increase in deposition of beta amyloid in cortex, or reducing the loss of cognitive or functional abilities, which comprises administering thereto a therapeutically acceptable dose of galantamine or a pharmaceutically acceptable salt thereof to a patient having medial temporal lobe, paralimbic, and/or temporoparietal lobe atrophy on structural MRI, or decreased fluorodeoxyglucose uptake in the temporoparietal cortices on PET scan.
20-21. (canceled)
A method which comprises administering a therapeutically acceptable dose of a compound of galantamine or a pharmaceutically acceptable salt thereof to a patient who has been determined to have the ApoE4 isoform of Apolipoprotein E or variants of BIN1, ABC7, PICALM, MS4A4E/MS4A6A, CD2AP, CD33, TREM2, EPBA1, CLU, CR1 and SORL1 or other gene variants associated with an increased risk for Alzheimer's dementia but who is not demented in an amount sufficient to inhibit plaque deposition or aid in removal of plaques of Aβ, or to maintain or increase levels of CSF Aβ42, or reduce progression of cognitive and/or functional decline, or delay progression to Alzheimer's dementia.
23-24. (canceled)
A method for maintaining or increasing levels of Aβ42 in CSF, reducing deposition of or removing Aβ42 from cortex, or delaying cognitive or functional decline in patients carrying fully penetrant mutations causing Alzheimer's dementia which comprises administering thereto a therapeutically acceptable dose of galantamine or a pharmaceutically acceptable salt thereof.
26-27. (canceled)
A method comprising administering a therapeutically acceptable dose of galantamine or a pharmaceutically acceptable salt thereof to a patient who is not demented in co-administration with an agent which promotes clearance by administering Aβ antibodies or stimulating antibody production, or binding or resulting in binding to Aβ species, including but not limited to solanezumab, aducanumab, ganterenumab, crenezumab, in order to enhance or slow the decline of cognitive and/or functional abilities, to enhance the decrease in cerebral Aβ deposits, or retard conversion to Alzheimer's dementia.
29-30. (canceled)
A method of administering a therapeutically acceptable dose of galantamine or a pharmaceutically acceptable salt thereof to a patient who is not demented, and is treated a BACE inhibitor, in order to maintain or increase levels of CSF Aβ, decrease elevated beta amyloid in brain, enhance performance on existing, composite or newly devised cognitive tests, reduce atrophy on structural MRI or reduce reductions in deoxyglucose uptake, or to reduce shrinkage of the brain.
32-33. (canceled)
35-36. (canceled)
Dependencies are inferred from the claim text.