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Neurodegenerative disorders are characterized by the progressive loss of specific populations of neurons with consequent deterioration of brain’s function and dramatic impact on human behavior. At present, there are no effective cures for neurodegenerative diseases. Because unambiguous diagnosis is possible only after manifestation of symptoms, when a large proportion of neurons has been already lost, therapies are necessarily confined to alleviation of symptoms. Development of cures halting the disease course is hampered by our rudimentary understanding of the etiopathology. Most neurodegenerative disorders are sporadic and age-related and - even for those of known genetic origin - the mechanisms influencing disease onset and progression have not been fully characterized. The different diseases, however, share important similarities in the mechanisms responsible for neuronal loss, which is caused by a combination of endogenous and exogenous challenges. Trophic deprivation, oxidative stress, accumulation of abnormal protein aggregates, and bioenergetics defects have been described in most, if not all, neurodegenerative disease.To counterbalance these noxious stimuli cells deploy, at least during the initial pathogenic states, intrinsic neuroprotective responses. These are general compensatory mechanisms, common to several neurodegenerative conditions, which reprogram cellular physiology to overcome stress. Adaptation includes strategies to optimize energetic resources, for instance reduction of rRNA synthesis to repress translation, suppression of transcription, and bioenergetics and metabolic redesign. Additional mechanisms include potentiation of antioxidant capacity, induction of endoplasmic reticulum (ER) stress, and activation of protein quality control systems and autophagy. Ineffective execution of these compensatory strategies severely threatens cellular homeostasis and favors onset of pathology. Therefore, a better understanding of these “buffering” mechanisms and of their interconnections may help to devise more effective therapeutic tools to prolong neuronal survival and activity, independently of the original genetic mutations and stress insults.This Research Topic focuses on the initial compensatory responses protecting against failure of those mechanisms that sustaining neuronal survival and activity. The collection intends to summarize the state-of-the-art in this field and to propose novel research contributes, with the ultimate goal of inspiring novel studies aimed to contrast progression of neurodegenerative diseases.

Nervous system --- Neuropsychiatry. --- Degeneration --- Research. --- models --- stress response --- Compensation --- mechanisms --- tran --- Neurodegenerative disorders

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Neuroimaging has become a crucial technique for Neurosciences. Different structural, functional and neurochemical methods, developed in recent decades, have allowed a systematic investigation on the role of neural substrates involved in functions performed by the central nervous system, whether normal or pathological. This book includes contributions from the general area of the neuroimaging to the understanding of normal functions and abnormalities of the central nervous system.

Nervous system --- Degeneration. --- Degeneration, Nerve --- Nerve degeneration --- Nervous system degeneration --- Neurodegenerative disease --- Neurodegenerative diseases --- Neurodegenerative disorders --- Neuron degeneration --- Nissl degeneration --- Retrograde degeneration --- Wallerian degeneration --- Degeneration (Pathology) --- Degeneration and regeneration --- Radiology

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The rate of technological progress is encouraging increasingly sophisticated lines of enquiry in cognitive neuroscience and shows no sign of slowing down in the foreseeable future. Nevertheless, it is unlikely that even the strongest advocates of the cognitive neuroscience approach would maintain that advances in cognitive theory have kept in step with methods-based developments. There are several candidate reasons for the failure of neuroimaging studies to convincingly resolve many of the most important theoretical debates in the literature. For example, a significant proportion of published functional magnetic resonance imaging (fMRI) studies are not well grounded in cognitive theory, and this represents a step away from the traditional approach in experimental psychology of methodically and systematically building on (or chipping away at) existing theoretical models using tried and tested methods. Unless the experimental study design is set up within a clearly defined theoretical framework, any inferences that are drawn are unlikely to be accepted as anything other than speculative. A second, more fundamental issue is whether neuroimaging data alone can address how cognitive functions operate (far more interesting to the cognitive scientist than establishing the neuroanatomical coordinates of a given function - the where question).

Nervous system --- Degeneration. --- Degeneration, Nerve --- Nerve degeneration --- Nervous system degeneration --- Neurodegenerative disease --- Neurodegenerative diseases --- Neurodegenerative disorders --- Neuron degeneration --- Nissl degeneration --- Retrograde degeneration --- Wallerian degeneration --- Degeneration (Pathology) --- Degeneration and regeneration --- Radiology

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Neurodegenerative disorders (NDs) are becoming more prevalent in our aging population, and traditional methods of monitoring ND symptoms can be challenging. Wearable technology offers several advantages, such as continuous monitoring, objective measurements, and remote monitoring. The present reprint includes a collection of eleven research and review articles that propose wearable solutions and explore signal processing, machine learning, and deep learning approaches for the computerized diagnosis and monitoring of NDs. Topics covered include using wearable technology to measure blood pressure, movement, sleep patterns, and brain activity, and developing predictive models to support clinicians in making informed decisions about treatment and care. This reprint is a valuable resource for anyone interested in the potential of wearable technology to improve the diagnosis and management of NDs.

Nervous system --- Degeneration. --- Degeneration, Nerve --- Nerve degeneration --- Nervous system degeneration --- Neurodegenerative disease --- Neurodegenerative diseases --- Neurodegenerative disorders --- Neuron degeneration --- Nissl degeneration --- Retrograde degeneration --- Wallerian degeneration --- Degeneration (Pathology) --- Degeneration and regeneration

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Inflammation of the brain in the context of neurodegenerative disorders is an area of intense debate and discussion, not least in terms of its pathogenic significance and the extent to which it drives disease processes and pathology. This inflammation can take several forms including innate responses involving microglia, humoral responses involving antibody, complement mediated processes and cellular T-cell activation, of which the role and extent of each may differ between diseases. Whilst some diseases have been more intensely linked to inflammation and long-term degeneration (e.g. MS), more traditional chronic neurodegenerative disorders have been thought of in terms of intrinsic neuronal pathology with a secondary innate response. However, it has been described that microglia activation is an early event of many degenerative disorders and evidence is accumulating that it may play a critical role in actually causing pathology and driving disease processes. If true, this would have major therapeutic implications, but what is the evidence that this is the case?The initial observations by Patrick McGeer’s group of post-mortem tissue from patients with Parkinson’s disease revealed the presence of activated brain microglia long-term and has thus lead to the hypothesis that chronic inflammation could participate to neuronal degenerative processes. The significance of these original observations has only been recently revisited, and the development of more powerful tools to study the brain immune response has certainly contributed to this field of research. Chronic inflammation in the brain can take many forms but of particular interest has been the resident microglia and the role they play in this process. In this context, microglia have often been thought to become activated only after the disease has begun and then to contribute minimally to the degenerative process. Emerging new concepts challenge this view by proposing that microglial senescence, for example, may release the disease process and/or accelerate it. In addition, microglia, once activated, can adopt different phenotypes which can be both pro-inflammatory and pro-repair and may impact not only on the healthy adult neuronal population but on those new neurons derived from neurogenic niches of the adult brain.In this Research Topic, we attempt to explore this by first considering the innate immune responses in the brain and the methods by which they can be studied experimentally and in patients with various neurodegenerative disorders. This sets the scene for then discussing a range of different disorders including Alzheimer’s, Parkinson’s, Huntington’s disease and amyotrophic lateral sclerosis. These papers seek to discuss the evidence for an innate immune response and whether this is beneficial or detrimental, as well as its therapeutic implications.

Natural immunity. --- Nervous system --- Degeneration. --- Disease resistance --- Host resistance --- Innate immunity --- Innate resistance --- Native immunity --- Natural resistance --- Nonspecific immunity --- Resistance to disease --- Immunity --- Degeneration, Nerve --- Nerve degeneration --- Nervous system degeneration --- Neurodegenerative disease --- Neurodegenerative diseases --- Neurodegenerative disorders --- Neuron degeneration --- Nissl degeneration --- Retrograde degeneration --- Wallerian degeneration --- Degeneration (Pathology) --- Degeneration and regeneration --- Therapeutics --- Inflammation --- Animal Models