Abstract: The present invention includes a method of inhibiting an activity of a BACE1 protein comprising contacting the BACE1 protein with a ligand that specifically inhibits residue Asp 32 of the human BACE1 protein.

Abstract: The present invention includes methods for detecting and reducing or inhibiting ischemic stroke in a mammal, the method comprising: (a) selecting microRNAs to downregulate selected from the group consisting of hsa-miR-96-5p, hsa-miR-99a-5p, hsa-miR-122-5p, hsa-miR-186-5p, hsa-miR-211-5p, hsa-mir-760, PC-3p-57664, or PC-5p-12969, (b) selecting microRNAs to upregulate selected from the group consisting of ggo-miR-139, hsa-miR-30d-5p, hsa-miR-22-3p, hsa-miR-23a-3p, mmu-miR-5124a, mmu-mir-6240-5p, PC-3p-32463, or PC-5p-211, and combinations thereof, and (c) administering an agent that: downregulates that targets in (a), upregulates the targets in (b), or both, to the subject in an amount sufficient to reduce or inhibit ischemic stroke in the mammal. The present invention also includes the detection of the markers for use with stroke patients.

Abstract: The present invention includes a method for identifying an Alzheimer's disease (AD) patient prior to reaching clinical disease classification, comprising: obtaining a dataset associated with a blood, serum, or plasma sample from the patient, wherein the dataset comprises data representing the level of one or more microRNA biomarkers in the blood, serum, or plasma sample; assessing the dataset for a presence or an increase in an amount of miRNA-455-3p; determining the likelihood that the patient will develop AD patient prior to reaching clinical disease classification by detecting the presence or the increase in miRNA-455-3p to produce a score that is indicative of a likelihood of developing AD, wherein a higher score relative to a healthy control indicates that the patient is likely to have the prognosis for transitioning to classified AD, wherein the healthy control is derived from a non-AD patient with no clinical evidence of AD.

Abstract: The present invention includes a method of inhibiting an activity of a BACE1 protein comprising contacting the BACE1 protein with a ligand that specifically inhibits residue Asp 32 of the human BACE1 protein.

Abstract: The present invention includes methods for detecting and reducing or inhibiting ischemic stroke in a mammal, the method comprising: (a) selecting microRNAs to downregulate selected from the group consisting of hsa-miR-96-5p, hsa-miR-99a-5p, hsa-miR-122-5p, hsa-miR-186-5p, hsa-miR-211-5p, hsa-mir-760, PC-3p-57664, orPC-5p-12969, (b) selecting microR-NAs to upregulate selected from the group consisting of ggo-miR-139, hsa-miR-30d-5p, hsa-miR-22-3p, hsa-miR-23a-3p, mmu-miR-5124a, mmu-mir-6240-5p, PC-3p-32463, or PC-5p-211, and combinations thereof, and (c) administering an agent that: downregulates that targets in (a), upregulates the targets in (b), or both, to the subject in an amount sufficient to reduce or inhibit ischemic stroke in the mammal. The present invention also includes the detection of the markers for use with stroke patients.

Abstract: The present invention includes a method for identifying an Alzheimer's disease (AD) patient prior to reaching clinical disease classification, comprising: obtaining a dataset associated with a blood, serum, or plasma sample from the patient, wherein the dataset comprises data representing the level of one or more microRNA biomarkers in the blood, serum, or plasma sample; assessing the dataset for a presence or an increase in an amount of miRNA-455-3p; determining the likelihood that the patient will develop AD patient prior to reaching clinical disease classification by detecting the presence or the increase in miRNA-455-3p to produce a score that is indicative of a likelihood of developing AD, wherein a higher score relative to a healthy control indicates that the patient is likely to have the prognosis for transitioning to classified AD, wherein the healthy control is derived from a non-AD patient with no clinical evidence of AD.

Abstract: The present invention includes a method of protecting neuronal cells from A?-induced toxicities in a subject comprising: providing the subject in need of treatment for an A?-induced toxicity with an agent that increases the miRNA-445-3p in the subject, wherein an increase in miR-455-3p expression in the neuronal cells enhances neuronal cell survival.

Abstract: The present invention includes a method of protecting neuronal cells from A?-induced toxicities in a subject comprising: providing the subject in need of treatment for an A?-induced toxicity with an agent that increases the miRNA-445-3p in the subject, wherein an increase in miR-455-3p expression in the neuronal cells enhances neuronal cell survival.

Abstract: The present invention includes a method for preventing or treating a disease or condition with excessive fragmentation of mitochondria or mitochondrial dysfunction comprising, consisting essentially of, or consisting of: identifying a subject suspected of needing treatment for excessive fragmentation of mitochondria or mitochondrial dysfunction; and administering to the subject with an amount of a mitochondrial division inhibitor 1 sufficient to prevent or treat the excessive fragmentation of mitochondria or mitochondrial dysfunction.