Abstract: Described herein are methods and compositions for treating Alzheimer's Disease (AD), as well as compositions comprising a reelin-derived peptide and methods of use thereof.

Abstract: Provide herein are methods of treating human patients with familial Alzheimer's disease that result in delayed in symptom onset and/or slowed cognitive decline by administering a humanized monoclonal anti-amyloid beta (A?) antibody.

Abstract: Methods and compositions for preventing or treating cognitive decline associated with dementia and/or mild cognitive impairment and/or neurodegeneration using antibodies, peptides, fusion proteins, or genome editing systems that modulate HSPG/heparin binding affinities of ApoE.

Abstract: Methods and compositions for preventing or treating cognitive decline associated with dementia and/or mild cognitive impairment and/or neurodegeneration using antibodies, peptides, fusion proteins, or genome editing systems that modulate HSPG/heparin binding affinities of ApoE.

Abstract: Methods and compositions for preventing or treating cognitive decline associated with dementia and/or mild cognitive impairment and/or neurodegeneration using antibodies, peptides, fusion proteins, or genome editing systems that modulate HSPG/heparin binding affinities of ApoE.

Abstract: The present invention provides compositions and methods useful in the diagnosis and treatment of a variety of cognitive impairments including vascular cognitive impairment and dementia, and Alzheimer's Disease. In one particular embodiment, the level of the neurofilament light protein and/or phosphorylated tau (e.g., p-tau181) is used to diagnose a cognitive impairment or monitor the efficacy of a therapy.

Abstract: Methods and compositions for preventing or treating cognitive decline associated with dementia and/or mild cognitive impairment and/or neurodegeneration using antibodies, peptides, fusion proteins, or genome editing systems that modulate HSPG/heparin binding affinities of ApoE.

Abstract: A method is disclosed to acquire imaging and non-imaging datasets from like objects. A linkage is found using a partial least squares (PLS) technique between imaging and non-imaging datasets. The linkage is then reduced to an expression of a single numerical assessment. The single numerical assessment is then used as an objective, quantified assessment of the differences and similarities between the objects. The data each dataset can be aspects of performance, physical characteristics, or measurements of appearance.

Abstract: For real persons at risk for Alzheimer's disease, a neurodegenerative disease, or brain aging, a measurement's rate of change can be characterized during or following the real persons' treatment with disease-preventing or neurological age-slowing therapy. For hypothetical persons similar to the real persons at risk for these conditions but who are not so treated, the measurement's rate of change can be characterized over a like time interval. The disease-preventing or age-slowing therapy's efficacy is suggested by a smaller measurement rate of change over the like time interval in the real persons treated than in the hypothetical persons not so treated, even in the absence of clinical decline over the time interval. Measurements of neurodegenerative disease progression will have significantly higher rates of change in persons clinically affected by or at risk for the disease than in those persons at lower risk for the neurodegenerative disease.