A method for detecting a neurological disease associated with cognitive impairment, wherein the extracellular domain of EphA4 is measured from a biological sample taken from a subject.

The invention discloses biomarkers for human autism. The invention provides methods for treating, preventing, and diagnosing human autism and autism-related disorders.

Methods of treating neuronal disorders, such as mechanical neuronal traumas and neurodegenerative disorders, with TWEAK or a TWEAK receptor blocking agents are presented.

The present disclosure provides methods of treating a tauopathy, involving administering an anti-Tau antibody. The present disclosure also provides anti-Tau antibodies, and formulations comprising same, for use in the methods.

Provided are novel human-derived dipeptide repeat (DPR) specific antibodies as well as synthetic variants and biotechnological derivatives thereof, preferably capable of binding C9ORF72 DPRs, as well as methods related thereto. Assays, kits, and solid supports related to antibodies specific for DPRs and DPR proteins such C9ORF72 DPRs are also disclosed. The antibody of the present invention can be used in pharmaceutical and diagnostic compositions for DPR protein-targeted immunotherapy and diagnostics.

The present relates to the use of miRNA-132/212 mimics or activators comprising a doubled stranded ribonucleic acid molecule comprising a seed region sequence of miRNA-132 or miRNA-212, a spacer, a stabilizing sequence, and a carrier for the treatment of neurodegenerative disorders, including Alzheimer's disease, Tauopathies, Amyotrophic lateral sclerosis, Parkinson's disease, frontotemporal dementia, prion's disease, mild cognitive impairment and Huntington's disease.

The presence of misfolded proteins in the brain is the hallmark of neurodegenerative diseases. Protein aggregates could have systemic expression and might be found in several tissues including the skin. This demonstrates the presence of phosphorylated Tau (p-Tau) in the skin cells of patients with Alzheimer's Disease (AD). Antibodies against p-Tau (PHF, phosphorylated at S296 and AT8, phosphorylated at S202) were assayed in biopsied tissue from the retro-auricular area in 49 subjects: 20 with AD, 12 with nondegenerative dementia and 17 age-matched controls. Light and confocal microscopies were employed to localize Tau protein by immunohistochemistry and their presence in the skin was confirmed through Western blots. The skin biopsy taken from AD patients presented significantly higher levels of p-Tau (AT8: hyperphosphorylated at Ser 202) when compared both to control subjects and patients with non-degenerative dementia (p<0.001). This study demonstrates the presence of p-Tau in skin biopsies by immunoreactivity. This procedure could be used to support the clinical diagnosis of AD in living patients.

The invention provides anti-Tau antibodies and methods of using the same.

The present invention refers to p53 sequence and post translational modifications (PTMs) and to their use as biomarkers in the diagnosis of neurodegenerative disease and cognitive decline and/or in the prognosis of Alzheimer's disease at different stages and/or of neurodegenerative disease in a biological sample. The invention also provides for a 1) diagnostic method based on a highly accurate mass spectrometry analysis for the diagnosis of neurodegenerative disease, including Mild Cognitive Impairment (MCI), Alzheimer's disease (AD), fronto-temporal dementia (FTD), Lewi's Body (LB), and vascular dementia (VD) in a subject, by evaluating the PTMs to the said p53 linear sequence protein and possible cut of its full sequence specifically in human plasma of patients; and 2) prognosis of AD in CU and MCI patients.

Alzheimer's disease, the most common cause of dementia in older individuals, is a debilitating neurodegenerative disease for which there is currently no cure. In the past, AD could only be definitively diagnosed by brain biopsy or upon autopsy after a patient died. These methods, which demonstrate the presence of the characteristic plaque and tangle lesions in the brain, are still considered the gold standard for the pathological diagnoses of AD. However, in the clinical setting brain biopsy is rarely performed and diagnosis depends on a battery of neurological, psychometric and biochemical tests, including the measurement of biochemical markers such as the ApoE and tau proteins or the beta-amyloid peptide in cerebrospinal fluid and blood. The present invention discloses and describes panels of makers that are differentially expressed in the disease state relative to their expression in the normal state and, in particular, identifies and describes panels of makers associated with neurocognitive disorders. Such biomarker panel might have considerable value in triaging patients with early memory disorders to yet more specific but more invasive and costly approaches such as molecular markers in CSF and on PET imaging in clinical trials and possibly in clinical practice.