Described herein are devices and methods for simultaneously expressing amyloid precursor protein and TonB protein. These devices and methods increase the production of these two proteins while also minimizing costs, making the proteins more widely accessible for medical research purposes, including the development of diagnostic tests for numerous diseases associated with elevated production of amyloid proteins. The amyloid precursor protein and TonB produced by the devices and methods described herein, as well as the devices themselves, can be used in experiments designed to model the interactions between metals and amyloids such as β-amyloid that are characteristic of numerous diseases such as Alzheimer's. Finally, provided herein are diagnostic tests that can detect Alzheimer's disease in samples from patients; the tests are sensitive enough to identify diseases such as Alzheimer's even at pre-clinical stages, before the appearance of symptoms.

The present disclosure provides methods to quantify tau phosphorylation at specific amino acid residues to predict time to onset of mild cognitive impairment due to Alzheimer's disease, stage Alzheimer's disease, guide treatment decisions, select subjects for clinical trials, and evaluate the clinical efficacy of certain therapeutic interventions.

A method for the pre-amplification sample processing of a prion or other amyloid converting protein in a sample. A key feature of the assay is its ability to amplify and thus detect small quantities of the abnormally folded ‘seed’ forms of misfolded proteins. The assay also opens up the ability to quantify the amount of “seed” present. The methods facilitate the early detection of diseases associated with misfolded proteins, as well as assessment of therapies against these diseases. The method can detect amyloid seeding activity (prions) in blood samples, including the buffy coat cells harvested from pre-clinical and clinical subjects. These findings further enhance the ability to assess the longitudinal course of prion disease and the role hematogenous prions play in pathogenesis. We demonstrate the ability to detect prions in as few as 5×10.sup.5 buffy coat cells by lipase-iron oxide bead-RT-QuIC performed at 42° C. (LIQ42) in 79% of CWD-biopsy positive WTD, which increased to 100% when LIQ was performed at 55° C. (LIQ55). RT-QuIC assessment of PMCA (PQ) round 5 product revealed hematogenous prions in 92% of the WTD.

Methods of diagnosis and methods of treatment and prevention for autism spectrum disorder are provided using decoy antigens to maternal brain-reactive antibodies.

A polytherapy of orally available compounds is disclosed that synergistically modulates and induces the expression of the cathelicidin gene (CAMP), which encodes the host defense peptide LL-37. By providing a number of different CAMP-inducing compounds together at the same time, stronger gene induction is achieved than with just one or two compounds, because the mechanism of induction broadens. Induction also may vary in different pas of the body depending on which compounds are used, and at what levels. We show for the first time that the polytherapy can induce cathelicidin expression in the brain, which may help to treat or prevent Alzheimer's Disease Systemic cathelicidin gene induction may help treat numerous other conditions including Type 2 Diabetes/Metabolic Syndrome, or chronic bacterial, viral, or fungal infections associated with increased cancer risk or neurodegeneration. By increasing cellular autophagy and macroautophagy and supporting mitochondrial biogenesis and homeostasis, CAMP gene upregulation may reduce the effects of cellular aging and increase longevity.

An in vitro method for diagnosing Alzheimer's disease (AD) includes determining the content of mercaptoalbumin (HMA) in a sample of cerebrospinal fluid (CSF), and comparing the content determined with the content of HMA in CSF in healthy subjects. If the HMA content is less than that of the healthy subjects, it is indicative of AD.

Methods of categorisation of schizophrenia sufferers into subtypes based on changes in brain morphology, together with associated blood biomarkers are provided. The methods allow for more accurate treatment and diagnosis of schizophrenia.

Described herein are deiminated proteins that are deiminated in response to oxygen-deprivation brain injury (ODBI) and/or oxygen-deprivation causing injury (ODCI). Also described are related methods and devices for detecting, diagnosing, and monitoring ODBI or ODCI, and methods for treating ODBI or ODCI.

The present disclosure provides treatments for neurodegenerative disorders and more particularly to methods for treatment of patients with Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), or Alzheimer's disease of different degrees of severity. The methods for treatment of patients who have suffered neurodegenerative diseases and specifically MS, ALS, or Alzheimer's disease includes administering a xenon gas mixture in subjects with elevated levels of neurodegenerative microglia (MGnD), e.g., determined based on levels of inflammatory biomarkers, measured in blood, serum and CSF, or levels of CLEC7A (Dectin-1)/Translocator Protein (TSPO) expression, e.g., measured using TSPO imaging.

The present invention relates to methods of diagnosis and therapy for neurodegenerative diseases and disorders.