Summary Epileptic activity is frequently associated with Alzheimer's disease; this association has therapeutic implications, because epileptic activity can occur at early disease stages and might contribute to pathogenesis. In clinical practice, seizures in patients with Alzheimer's disease can easily go unrecognised because they usually present as non-motor seizures, and can overlap with other symptoms of the disease. In patients with Alzheimer's disease, seizures can hasten cognitive decline, highlighting the clinical relevance of early recognition and treatment. Some evidence indicates that subclinical epileptiform activity in patients with Alzheimer's disease, detected by extended neurophysiological monitoring, can also lead to accelerated cognitive decline. Treatment of clinical seizures in patients with Alzheimer's disease with select antiepileptic drugs (AEDs), in low doses, is usually well tolerated and efficacious. Moreover, studies in mouse models of Alzheimer's disease suggest that certain classes of AEDs that reduce network hyperexcitability have disease-modifying properties. These AEDs target mechanisms of epileptogenesis involving amyloid β and tau. Clinical trials targeting network hyperexcitability in patients with Alzheimer's disease will identify whether AEDs or related strategies could improve their cognitive symptoms or slow decline.

Epileptic activity in Alzheimer's disease: causes and clinical relevance

Gut microbiota has a proven role in regulating multiple neuro-chemical pathways through the highly interconnected gut-brain axis Oral bacteriotherapy thus has potential in the treatment of central nervous system-related pathologies, such as Alzheimer’s disease (AD) Current AD treatments aim to prevent onset, delay progression and ameliorate symptoms In this work, 3xTg-AD mice in the early stage of AD were treated with SLAB51 probiotic formulation, thereby affecting the composition of gut microbiota and its metabolites This influenced plasma concentration of inflammatory cytokines and key metabolic hormones considered therapeutic targets in neurodegeneration Treated mice showed partial restoration of two impaired neuronal proteolytic pathways (the ubiquitin proteasome system and autophagy) Their cognitive decline was decreased compared with controls, due to a reduction in brain damage and reduced accumulation of amyloid beta aggregates Collectively, our results clearly prove that modulation of the microbiota induces positive effects on neuronal pathways that are able to slow down the progression of Alzheimer’s disease

/pdf/microbiota-modulation-counteracts-alzheimer-s-disease-2gm0ra9dbh.pdf

Microbiota modulation counteracts Alzheimer's disease progression influencing neuronal proteolysis and gut hormones plasma levels.

Progress toward the development of efficacious therapies for Alzheimer's disease (AD) is halted by a lack of understanding early underlying pathological mechanisms. Systems biology encompasses several techniques including genomics, epigenomics, transcriptomics, proteomics, and metabolomics. Metabolomics is the newest omics platform that offers great potential for the diagnosis and prognosis of neurodegenerative diseases as an individual's metabolome reflects alterations in genetic, transcript, and protein profiles and influences from the environment. Advancements in the field of metabolomics have demonstrated the complexity of dynamic changes associated with AD progression underscoring challenges with the development of efficacious therapeutic interventions. Defining systems-level alterations in AD could provide insights into disease mechanisms, reveal sex-specific changes, advance the development of biomarker panels, and aid in monitoring therapeutic efficacy, which should advance individualized medicine. Since metabolic pathways are largely conserved between species, metabolomics could improve the translation of preclinical research conducted in animal models of AD into humans. A summary of recent developments in the application of metabolomics to advance the AD field is provided below.

/pdf/application-of-metabolomics-in-alzheimer-s-disease-o5m6wctadf.pdf

Application of Metabolomics in Alzheimer's Disease.

Taurine is a sulfur-containing amino acid and known as semi-essential in mammals and is produced chiefly by the liver and kidney. It presents in different organs, including retina, brain, heart and placenta and demonstrates extensive physiological activities within the body. In the several disease models, it attenuates inflammation- and oxidative stress-mediated injuries. Taurine also modulates ER stress, Ca2+ homeostasis and neuronal activity at the molecular level as part of its broader roles. Different cellular processes such as energy metabolism, gene expression, osmosis and quality control of protein are regulated by taurine. In addition, taurine displays potential ameliorating effects against different neurological disorders such as neurodegenerative diseases, stroke, epilepsy and diabetic neuropathy and protects against injuries and toxicities of the nervous system. Several findings demonstrate its therapeutic role against neurodevelopmental disorders, including Angelman syndrome, Fragile X syndrome, sleep-wake disorders, neural tube defects and attention-deficit hyperactivity disorder. Considering current biopharmaceutical limitations, developing novel delivery approaches and new derivatives and precursors of taurine may be an attractive option for treating neurological disorders. Herein, we present an overview on the therapeutic potential of taurine against neurological disorders and highlight clinical studies and its molecular mechanistic roles. This article also addresses the neuropharmacological potential of taurine analogs.

Taurine and its analogs in neurological disorders: Focus on therapeutic potential and molecular mechanisms

Amyloid-β (Aβ) is a major pathological mediator of both familial and sporadic Alzheimer's disease (AD). In the brains of AD patients, progressive accumulation of Aβ oligomers and plaques is observed. Such Aβ abnormalities are believed to block long-term potentiation, impair synaptic function, and induce cognitive deficits. Clinical and experimental evidences have revealed that the acute increase of Aβ levels in the brain allows development of Alzheimer-like phenotypes. Hence, a detailed protocol describing how to acutely generate an AD mouse model via the intracerebroventricular (ICV) injection of Aβ is necessary in many cases. In this protocol, the steps of the experiment with an Aβ-injected mouse are included, from the preparation of peptides to the testing of behavioral abnormalities. The process of preparing the tools and animal subjects before the injection, of injecting the Aβ into the mouse brain via ICV injection, and of assessing the degree of cognitive impairment are easily explained throughout the protocol, with an emphasis on tips for effective ICV injection of Aβ. By mimicking certain aspects of AD with a designated injection of Aβ, researchers can bypass the aging process and focus on the downstream pathology of Aβ abnormalities.

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits.

Alzheimer's disease (AD) is a lethal progressive neurological disorder affecting the memory. Recently, US Food and Drug Administration mitigated the standard for drug approval, allowing symptomatic drugs that only improve cognitive deficits to be allowed to accelerate on to clinical trials. Our study focuses on taurine, an endogenous amino acid found in high concentrations in humans. It has demonstrated neuroprotective properties against many forms of dementia. In this study, we assessed cognitively enhancing property of taurine in transgenic mouse model of AD. We orally administered taurine via drinking water to adult APP/PS1 transgenic mouse model for 6 weeks. Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice. In the cortex of APP/PS1 mice, taurine slightly decreased insoluble fraction of Aβ. While the exact mechanism of taurine in AD has not yet been ascertained, our results suggest that taurine can aid cognitive impairment and may inhibit Aβ-related damages.

/pdf/taurine-in-drinking-water-recovers-learning-and-memory-in-cv9pyjaacc.pdf

Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease

Parkinson's disease (PD) is a neurodegenerative disease that affects motor abilities with increasing severity as the disease progresses. Traditional methods for diagnosing PD include a section where a trained specialist scores qualitative symptoms using the motor subscale of the Unified Parkinson's Disease Rating Scale (UPDRS-III). The aim of this feasibility study was twofold. First, to evaluate quiet standing as an additional, out-of-clinic, objective feature to predict UPDRS-III subscores related to motor symptom severity; and second, to use quiet standing to detect the presence of motor symptoms. Force plate data were collected from 42 PD patients and 43 healthy controls during quiet standing (a task involving standing still with eyes open and closed) as a feasible task in clinics. Predicting each subscore of the UPDRS-III could aid in identifying progression of PD and provide specialists additional tools to make an informed diagnosis. Random Forest feature importance indicated that features correlated with range of center of pressure (i.e., the medial-lateral and anterior-posterior sway) were most useful in the prediction of the top PD prediction subscores of postural stability (r = 0.599; p = 0.014), hand tremor of the left hand (r = 0.650; p = 0.015), and tremor at rest of the left upper extremity (r = 0.703; p = 0.016). Quiet standing can detect body bradykinesia (AUC-ROC = 0.924) and postural stability (AUC-ROC = 0.967) with high predictability. Although there are limited data, these results should be used as a feasibility study that evaluates the predictability of individual UPDRS-III subscores using quiet standing data.

Predicting UPDRS Motor Symptoms in Individuals With Parkinson's Disease From Force Plates Using Machine Learning

Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer’s disease

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Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease

Predicting UPDRS Motor Symptoms in Individuals With Parkinson's Disease From Force Plates Using Machine Learning

Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer’s disease