| 1. |
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| 2. |
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| 3. |
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| 4. |
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| 5. |
- Wimo, A, et al.
(författare)
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Economical aspects of dementia
- 2008
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Ingår i: Handbook of clinical neurology. - 0072-9752. ; 89, s. 137-46
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Tidskriftsartikel (refereegranskat)
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| 6. |
- Zetterberg, Henrik, 1973, et al.
(författare)
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Biological CSF Markers of Alzheimer's Disease.
- 2008
-
Ingår i: Handbook of clinical neurology / edited by P.J. Vinken and G.W. Bruyn. - 0072-9752. ; 89, s. 261-8
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Tidskriftsartikel (refereegranskat)
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| 7. |
- Alafuzoff, Irina, et al.
(författare)
-
Alpha-synucleinopathies.
- 2017
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752 .- 2212-4152. ; 145, s. 339-353
-
Tidskriftsartikel (refereegranskat)abstract
- A neurodegenerative disorder displaying an altered α-synuclein (αS) in the brain tissue is called α-synucleinopathy (αS-pathy) and incorporates clinical entities such as Parkinson disease (PD), PD with dementia, dementia with Lewy bodies, and multiple-system atrophy. Neuroradiologic techniques visualizing αS pathology in the brain or assays of αS in the cerebrospinal fluid or blood are probably available and will be implemented in the near future but currently the definite diagnosis of αS-pathy relies on a postmortem examination of the brain. Since the 1980s immunohistochemical technique based on the use of antibodies directed to proteins of interest has become a method of choice for neuropathologic diagnosis. Furthermore, since the 1990s it has been acknowledged that progressions of most neurodegenerative pathologies follow a certain predictable time-related neuroanatomic distribution. Currently, for Lewy body disease, two staging techniques are commonly used: McKeith and Braak staging. Thus, the neuropathologic diagnosis of a αS-pathy is based on detection of altered αS in the tissue and registration of the neuroanatomic distribution of this alteration in the brain. The clinicopathologic correlation is not absolute due to the quite frequent observation of incidental and concomitant αS pathology.
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| 8. |
- Alafuzoff, Irina, et al.
(författare)
-
Comorbidities.
- 2017
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752 .- 2212-4152. ; 145, s. 573-577
-
Tidskriftsartikel (refereegranskat)abstract
- The term comorbidities or mixed pathologies is used when brain tissue, a surgical sample, or postmortem brain displays a mixture of protein alterations or other pathologies. Most of the alterations when seen in sufficient extent are considered causative, are related to a certain clinical phenotype, i.e., when hyperphosphorylated τ (HPτ) is observed in occipital cortex concomitant with β-amyloid (Aβ), the diagnosis is Alzheimer disease (AD). When HPτ is observed in hippocampal structures in a subject with extensive and widespread α-synuclein pathology, a Lewy body disease (LBD), the HPτ pathology is considered as a concomitant alteration. There are numerous reports indicating that when "concomitant" pathologies are seen in a subject with certain neurodegenerative diseases, the clinical phenotype might be altered. In addition there are those cases where many alterations are seen in a sparse extent, but jointly they lead to a clinical syndrome. Thus today it is not sufficient to confirm a certain pathology to be seen, i.e., AD- or LBD-related; in addition the concomitant aging-related alterations have to be looked for.
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| 9. |
- Alafuzoff, Irina
(författare)
-
Minimal neuropathologic diagnosis for brain banking in the normal middle-aged and aged brain and in neurodegenerative disorders.
- 2018
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752 .- 2212-4152. ; 150, s. 131-141
-
Tidskriftsartikel (refereegranskat)abstract
- Research on human brain diseases is currently often conducted on cell cultures and animals. Several questions however can only be addressed by studying human postmortem brain tissue. However, brain tissue obtained postmortem almost always displays pathology that is often related to the aging phenomenon. Thus, in order to be certain that the answers obtained are reliable, a systematic and thorough assessment of the brain tissue to be studied should be carried out. We are currently aware of several protein alterations that are found in middle-aged and aged brains that are obtained from neurologically unimpaired subjects. The most common alteration is hyperphosphorylation of τ, observed in both neurons and glial cells, in certain brain regions, followed by β-amyloid aggregation in the neuropil and vessel walls. Less common protein alterations are those noted for α-synuclein and Tar DNA-binding protein 43. It is noteworthy that these alterations, when found in excess, are diagnostic for various neurodegenerative diseases, such as Alzheimer disease, Pick disease, progressive supranuclear palsy, corticobasal degeneration, Parkinson disease, Lewy body dementia, and frontotemporal lobar degeneration. Since 1990, the neuropathology community has been aware that these protein alterations tend to progress in an orderly neuroanatomically defined manner and have thus designed a method to define a stage or a phase of the protein alteration. The neuropathology community has defined an initiation site, or neuroanatomic area that they presume the alteration originates from, and defined a presumed pattern of progression from the initiation site to other brain areas. Thus a reliable and reproducible description of each case regarding these alterations can be achieved. In addition to the above alterations, the brain tissue is also prone to various vascular alterations that should be registered as seen or not seen even if the significance of these alterations is still unclear.
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| 10. |
- Alafuzoff, Irina
(författare)
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Techniques in neuropathology.
- 2017
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752 .- 2212-4152. ; 145, s. 3-7
-
Tidskriftsartikel (refereegranskat)abstract
- The primary objective for a neuropathologist is the characterization of the tissue that is being assessed and thus all available techniques ranging from naked-eye examination to assessment of genetic/epigenetic characteristics are currently applied. What is observed in the tissue obtained from a diseased subject is compared with what is observed in a healthy individual and, based on the outcome, neuropathologic definitions of diseases are constructed. Thus, with the naked eye a neuropathologist can confirm that a hemorrhage is observed in the brain, by histologic examination that the hemorrhage is caused by alterations in the brain vessels and, since 1954, applying Congo red dye neuropathologists have been able to state that congophilic angiopathy is detected. Since 1984, applying immunohistochemical methods neuropathologists have been able to verify that the protein seen in the vessel walls is β-amyloid and by genetic/epigenetic analysis eventual mutation or modifications of genome might be detected. The development of new techniques is staggering and throughout this book the authors have listed techniques currently applied while assessing various disease-related hallmark lesions. In the following a general summary of techniques applied is given.
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| 11. |
- Appelros, Peter, et al.
(författare)
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Sex differences in stroke.
- 2020
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752 .- 2212-4152. ; 175, s. 299-312
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Sex disparities within the field of stroke, including subarachnoid hemorrhages (SAHs), have been in focus during the last 2 decades. It is clear that stroke incidence is higher in men, and also that men have their first stroke earlier than women. On the other hand, women have more severe strokes, mainly because cardioembolic strokes are more common in women. This leads to higher case fatality and worse functional outcome in women. It has often been pointed out that women more often have nontraditional stroke symptoms, and therefore may seek medical help later. After discharge from the hospital, female stroke survivors live alone in many cases and are dependent on external care. Therefore, these women frequently rate their quality of life (QoL) lower than men do. Female spouses more often provide help to their male stroke survivors than the reverse, and they accept a heavier burden. These caregivers are at high risk for depression, low QoL, and low psychologic wellbeing. SAH is a special form of stroke, often caused by a ruptured aneurysm. It is about 20% more common in women. The case fatality is high, but does not differ between the sexes.
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| 12. |
- Barker, Roger A., et al.
(författare)
-
Restorative cell and gene therapies for Parkinson's disease
- 2023
-
Ingår i: Precision Medicine in Neurodegenerative Disorders, Part II. - 2212-4152 .- 0072-9752. - 9780323855556 ; 193, s. 211-226
-
Bokkapitel (refereegranskat)abstract
- One of the core pathological features of Parkinson's disease (PD) is the loss of the dopaminergic nigrostriatal pathway which lies at the heart of many of the motor features of this condition as well as some of the cognitive problems. The importance of this pathological event is evident through the clinical benefits that are seen when patients with PD are treated with dopaminergic agents, at least in early-stage disease. However, these agents create problems of their own through stimulation of more intact dopaminergic networks within the central nervous system causing major neuropsychiatric problems including dopamine dysregulation. In addition, over time the nonphysiological stimulation of striatal dopamine receptors by L-dopa containing drugs leads to the genesis of L-dopa-induced dyskinesias that can become very disabling in many cases. As such, there has been much interest in trying to better reconstitute the dopaminergic nigrostriatal pathway using either factors to regrow it, cells to replace it, or gene therapies to restore dopamine transmission in the striatum. In this chapter, we lay out the rationale, history and current status of these different therapies as well as highlighting where the field is heading and what new interventions might come to clinic in the coming years.
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| 13. |
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| 14. |
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| 15. |
- Dupuis, Luc, et al.
(författare)
-
Thermoregulation in amyotrophic lateral sclerosis
- 2018
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752 .- 2212-4152. ; 157, s. 749-760
-
Bokkapitel (refereegranskat)abstract
- Amyotrophic lateral sclerosis (ALS) is the major adult-onset motor neuron disease, and is clinically, pathologically, and genetically associated with frontotemporal dementia, the second cause of dementia in the elderly. Here, we review the evidence linking thermoregulation and ALS. Indeed, while ALS is not classically associated with defective thermoregulatory function, its progression severely affects key brain regions controlling body temperature and impacts multiple sensors and effectors of this homeostatic function. Furthermore, animal models of ALS display disturbed thermoregulation as a consequence of disrupted energy homeostasis. All these lines of indirect evidence call for studies directly addressing the body temperature regulatory system, both as a potential biomarker and as a possible modifier of disease progression in ALS.
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| 16. |
- Erfurth, Eva Marie
(författare)
-
Uncertainties in endocrine substitution therapy for central endocrine insufficiencies: growth hormone deficiency.
- 2014
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752. ; 124, s. 407-416
-
Tidskriftsartikel (refereegranskat)abstract
- The growth hormone deficiency (GHD) syndrome is associated with several metabolic abnormalities and it has been postulated that the increased cardiovascular disease (CVD) morbidity and mortality in GHD patients may be related to the missing metabolic effects of GH. Many CVD risk factors show improvements after GH therapy. Reduced bone mineral density (BMD) has been recorded both in patients with isolated GHD and in those with multiple pituitary deficiencies, indicating that GHD per se is responsible for the low BMD in both types of patients. These matters are, however, more complicated, as hypopituitary patients with GHD may have different phenotypes due to differences in underlying diagnoses. These phenotypes may not be clear-cut in individual patients. Moreover, patients may transit between different phenotypes over time due to extension of the pathology in the pituitary and/or the consequences of the treatment (surgery and/or radiotherapy). Three different phenotypes of hypopituitary patients will be discussed, with a focus on CVD risk and bone health: (1) patients with isolated GHD, e.g. due to prophylactic cranial radiotherapy for lymphoblastic leukaemia in childhood; (2) patients with GHD and multiple hormone deficiencies due to pituitary macroadenomas treated by surgery; (3) patients with GHD caused by craniopharyngiomas with multiple hormone deficiencies and hypothalamic involvement, where hypothalamic damage frequently dominates the positive metabolic effects of GH therapy. These phenotypes illustrate the differential impact of various pituitary pathologies on the phenotype of patients with GHD.
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| 17. |
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| 18. |
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| 19. |
- Fernell, Elisabeth, 1948, et al.
(författare)
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Borderline intellectual functioning
- 2020
-
Ingår i: Handbook of Clinical Neurology.. - : Elsevier. - 0072-9752. ; , s. 77-81
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Borderline intellectual functioning (BIF), that is to say, tested IQ levels in the range of 70–84/85, is prevalent, affecting about 12%–14% of the population depending on the exact level for “diagnostic” cutoff. In the current Diagnostic and Statistical Manual of Mental Disorders, BIF does not have a separate diagnostic category but can be categorized with a V-code. Children and adolescents with BIF usually struggle both as regards school performance and in respect of social functioning. BIF is common in attention deficit hyperactivity disorder, but sometimes attention problems in schoolchildren with BIF may be a consequence of nonadapted academic demands. Autism and BIF may also coexist, and there are many cases of so-called high-functioning autism who are high functioning only in the sense that they do not meet criteria for intellectual disability, but function in the area of BIF. Currently, too little attention is given to the negative effects of BIF on child development and adaptation. Learning, academic, and behavioral problems and grade retention may be markers of BIF. Our diagnostic and classification manuals need to have specific categories that clarify the problems that BIF entails so that affected individuals can avail themselves of better educational support and understanding. © 2020 Elsevier B.V.
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| 20. |
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| 21. |
- Illes, Sebastian
(författare)
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More than a drainage fluid: the role of CSF in signaling in the brain and other effects on brain tissue
- 2017
-
Ingår i: Cerebrospinal Fluid in Neurologic Disorders. Handbook of Clinical Neurology. - : Elsevier. - 0072-9752. - 9780128042793 ; , s. 33-46
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Current progress in neuroscience demonstrates that the brain is not an isolated organ and is influenced by the systemic environment and extracerebral processes within the body. In view of this new concept, blood and cerebrospinal fluid (CSF) are important body fluids linking extracerebral and intracerebral processes. For decades, substantial evidence has been accumulated indicating that CSF modulates brain states and influences behavior as well as cognition. This chapter provides an overview of how CSF directly modulates the function of different types of brain cells, such as neurons, neural stem cells, and CSF-contacting cells. Alterations in CSF content occur in most pathologic central nervous system (CNS) conditions. In a classic view, the function of CSF is to drain waste products and detrimental factors derived from diseased brain parenchyma. This chapter presents examples for how intra- and extracerebral pathologic processes lead to alterations in the CSF content. Current knowledge about how pathologically altered CSF influences the functionality of brain cells will be presented. Thereby, it becomes evident that CSF has more than a drainage function and has a causal role for the etiology and pathogenesis of different CNS diseases. © 2017 Elsevier B.V.
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| 22. |
- Kovacs, Gabor G, et al.
(författare)
-
Preface.
- 2017
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752 .- 2212-4152. ; 145, s. 9-
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Tidskriftsartikel (refereegranskat)
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| 23. |
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| 24. |
- Kyllerman, Mårten, 1941
(författare)
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Angelman syndrome.
- 2013
-
Ingår i: Handbook of clinical neurology. - 0072-9752. ; 111, s. 287-90
-
Tidskriftsartikel (refereegranskat)abstract
- Angelman syndrome combines severe mental retardation, epilepsy, ataxia, speech impairment, and unique behavior with happy demeanor, laughing, short attention span, hyperactivity, and sleep disturbance. Occurrence has been calculated at 1:20000 to 1:12000 constituting about 6% of all children with severe mental retardation and epilepsy. The physical "prototype" includes microcephaly with flat neck, fair skin and hair, wide-spaced teeth, and open mouth with tongue protrusion. Epilepsy is characterized by atypical absences, erratic myoclonus, and occasional tonic-clonic seizures. EEG demonstrates high-amplitude 2-3Hz delta activity with spike and slow-wave discharges and sleep-activated generalized epileptiform discharges. Sodium valproate, benzodiazepines, and priacetam are frequently used and effective. Development is generally slow, the majority attaining independent walking in the first 2.5-6 years. Vocabulary is limited to a few single words with superior speech and object apprehension. The condition is due to a lack of expression of the UBE3A gene on chromosome 15q. Maternal deletions of 15q11-13 produce the most pronounced phenotype (65-70% of probands), uniparental disomy and imprinting center mutations (10%), and UBE3A point mutations (11%) produce milder phenotypes.
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| 25. |
- Larsson, Elna-Marie, et al.
(författare)
-
Overview of neuroradiology.
- 2017
-
Ingår i: Handbook of Clinical Neurology. - 0072-9752 .- 2212-4152. ; 145, s. 579-599
-
Tidskriftsartikel (refereegranskat)abstract
- Neuroradiology with computed tomography (CT) and magnetic resonance imaging (MRI) is essential for the initial evaluation of patients with a clinical suspicion of brain and spine disorders. Morphologic imaging is required to obtain a probable diagnosis to support the treatment decisions in pre- and perinatal disorders, vascular diseases, traumatic injuries, metabolic disorders, epilepsy, infection/inflammation, neurodegenerative disorders, degenerative spinal disease, and tumors of the central nervous system. Different postprocessing tools are increasingly used for three-dimensional visualization and quantification of lesions. Additional information is provided by angiographic methods and physiologic CT and MRI techniques, such as diffusion MRI, perfusion CT/MRI, MR spectroscopy, functional MRI, tractography, and nuclear medicine imaging methods. Positron emission tomography (PET) is now integrated with CT (PET/CT), and PET/MR scanners have recently also been introduced. These hybrid techniques facilitate the co-registration of lesions with different modalities, and give new possibilites for functional imaging. Repeated imaging is increasingly performed for treatment monitoring. The improved imaging techniques together with the neuropathologic diagnosis after biopsy or surgery allow more personalized treatment of the patient. Neuroradiology also includes endovascular treatment of aneurysms and arteriovenous malformations as well as thrombectomy in acute stroke. This catheter-based treatment has replaced invasive neurosurgery in many cases.
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| 26. |
- Lindquist, L
(författare)
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Tick-borne encephalitis
- 2014
-
Ingår i: Handbook of clinical neurology. - 0072-9752. ; 123, s. 531-59
-
Tidskriftsartikel (refereegranskat)
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| 27. |
- Magnusson, Måns, et al.
(författare)
-
The conundrum of cervicogenic dizziness
- 2016
-
Ingår i: Handbook of Clinical Neurology. - 2212-4152 .- 0072-9752. ; 137, s. 365-369
-
Bokkapitel (refereegranskat)abstract
- Cervicogenic or cervical dizziness is debated as an entity. However, there exists both a physiologic basis and a multitude of clinical data to make such a disease concept at least possible and worth considering. In addition, the interaction of proprioceptive and vestibular mechanisms may amplify dizziness of other origin. Cervical pain and dizziness are both common symptoms and may coincide, and neck pain or obvious dysfunction does not necessarily cause dizziness or balance disturbances. So far, there is also the lack of a proper diagnostic test for cervicogenic dizziness. On the other hand, there is growing evidence that cervical proprioceptive input is important for balance and postural control not only in animals but also in humans, and that intervention in disorders affecting the human cervical segment may relieve dizziness in some patients. It is advocated that the diagnosis should be used with care and that there is a need for better diagnostic tests. In the absence of such a test, one has to rely on preliminary criteria and a diagnosis ex juvantibus. A possible approach would require patients to present with neck pain before or in close temporal relation with dizziness; that other causes should be made at least unlikely; and that treatment of a cervical dysfunction reduces also dizziness or balance disturbance.
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| 28. |
- Mathiesen, T
(författare)
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Parasagittal meningiomas
- 2020
-
Ingår i: Handbook of clinical neurology. - 0072-9752. ; 170, s. 93-100
-
Tidskriftsartikel (refereegranskat)
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| 29. |
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| 30. |
- Reus, Victor I., et al.
(författare)
-
Psychiatric manifestations of neurologic diseases : Etiology, phenomenology, and treatment
- 2019
-
Ingår i: Handbook of Clinical Neurology. - 2212-4152 .- 0072-9752. ; 165, s. 1-4
-
Bokkapitel (refereegranskat)abstract
- Understanding the etiology and meaning of behavioral symptomatology in the context of neurologic disease, and choosing the most effective intervention is a vexing task. This introduction summarizes the history of our understanding of the relationship between behavioral symptoms and primary neurologic conditions, and considers the ways in which both psychiatric and neurologic disorders occurring simultaneously may inform both knowledge of etiology and treatment decisions.
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| 31. |
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| 32. |
- Sacuiu, Simona Florentina, 1971
(författare)
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Dementias
- 2016
-
Ingår i: Handbook of Clinical Neurology 3rd series. - : Elsevier. - 0072-9752. - 9780128029732 ; , s. 123-51
-
Bokkapitel (refereegranskat)abstract
- This chapter will focus on the descriptive, analytic, and intervention-oriented epidemiology of dementia and its most frequent etiologic type due to Alzheimer's disease. The chapter opens with a brief presentation of the concept of dementia, followed by the presentation of dementia of the Alzheimer type (DAT), including natural history, clinical manifestation, neuropathology, medical prognosis, and management. Further, the chapter presents the prevalence and incidence of dementia, with special consideration of secular trends in prevalence and incidence of DAT, and prognosis of the socioeconomic impact of dementia. Thereafter the main risk factors for DAT are covered. The chapter also addresses the results of ongoing therapeutic and preventive intervention trials for DAT. Finally, the future challenges of the epidemiology of dementia with a focus on the impact of the new diagnostic criteria for neurocognitive disorders, as well as the development of biomarkers for DAT and other types of dementia, will be briefly discussed.
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| 33. |
- Sjörs Dahlman, Anna, 1981-, et al.
(författare)
-
The hypothalamo–pituitary–adrenal axis and the autonomic nervous system in burnout
- 2021
-
Ingår i: Handbook of Clinical Neurology. - : Elsevier B.V.. - 0072-9752. ; , s. 83-94, s. 83-94
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Burnout constitutes a serious health concern in the modern working environment. It is a stress-related condition that has developed as a result of a prolonged psychosocial stress exposure causing a persistent mismatch between demands and resources. The main symptom is emotional exhaustion, but physical fatigue, diminished professional efficacy, cynicism, and cognitive impairments are also associated with this condition. Burnout has been used both as a psychologic term in occupational settings and as a clinical diagnosis in patient populations, and there is currently no universally accepted definition and diagnostic criteria of burnout. It has been hypothesized that the two main stress response systems, the autonomic nervous system (ANS) and the hypothalamus–pituitary–adrenal axis (HPA axis), are involved in the pathogenesis of burnout. A common hypothesis is that in the early stages of chronic stress, the HPA axis and sympathetic ANS activity tend to be higher, while it will decrease with a longer duration of chronic stress to ultimately reach a state of hypoactivity in clinical burnout. The current research in this field shows many contradictory results. Thus there is no compelling evidence of either ANS or HPA dysfunction in burnout. However, there is partial support for the hypothesis of HPA and sympathetic hyperactivity in early stages, and HPA hyporeactivity and low vagal activity in more severe burnout cases, but high-quality studies investigating the causal links are still lacking. © 2021 Elsevier B.V.
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| 34. |
- Solheim, Ole, et al.
(författare)
-
Quality of life outcomes in meningioma surgery.
- 2020
-
Ingår i: Handbook of clinical neurology. Vol. 170. - : Elsevier. - 0072-9752. ; , s. 311-321
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Patient-reported quality of life measures hold the potential to capture the results of meningioma surgery in a more patient-centered and sensitive way than common morbidity measures. However, quality of life measures have not so far been used much in meningioma studies. Disease specific instruments are also lacking along with validation studies in patients with meningioma. While patient-reported quality of life measures may overestimate improvements and underestimate surgery-related deteriorations, quality of life studies still report worse outcomes than the common retrospective review of hospital records. A more widespread use of longitudinal assessment of quality of life would also have the benefit in moving meningioma research from retrospective to prospective, which would lead to superior data quality. Comparisons across studies would also be more valid as the assessment bias resulting from surgeons judging their own results would be avoided.
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| 35. |
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| 36. |
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| 37. |
- Weydt, Patrick, et al.
(författare)
-
Thermoregulatory disorders in Huntington disease
- 2018
-
Ingår i: Handbook of Clinical Neurology. - 2212-4152 .- 0072-9752. ; 157, s. 761-775
-
Bokkapitel (refereegranskat)abstract
- Huntington disease (HD) is a paradigmatic autosomal-dominant adult-onset neurodegenerative disease. Since the identification of an abnormal expansion of a trinucleotide repeat tract in the huntingtin gene as the underlying genetic defect, a broad range of transgenic animal models of the disease has become available and these have helped to unravel the relevant molecular pathways in unprecedented detail. Of note, some of the most informative of these models develop thermoregulatory defects such as hypothermia, problems with adaptive thermogenesis, and an altered circadian temperature rhythm. Both central, e.g., in the hypothalamus and peripheral, i.e., the brown adipose tissue and skeletal muscle, problems contribute to the phenotype. Importantly, these structures and pathways are also affected in human HD. Yet, currently the evidence for bona fide thermodysregulation in human HD patients remains anecdotal. This may be due to a lack of reliable tools for monitoring body temperature in an outpatient setting. Regardless, study of the temperature phenotype has contributed to the identification of unexpected molecular targets, such as the PGC-1α pathway.
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| 38. |
- Zetterberg, Henrik, 1973, et al.
(författare)
-
Cerebrospinal fluid in the dementias.
- 2017
-
Ingår i: Handbook of clinical neurology. - 0072-9752. ; 146, s. 85-97
-
Tidskriftsartikel (refereegranskat)abstract
- Alzheimer disease, vascular dementia, dementia with Lewy bodies, and frontotemporal dementia are the most common central nervous system disorders that cause progressive neurocognitive dysfunction and ultimately dementia. A number of biomarkers for pathologies reflecting each condition have been developed. Here, we review these and give an overview of the current state of practice and research regarding cerebrospinal fluid biomarkers for these disorders. The chapter discusses both established (most of which are tau- and amyloid β-related) and upcoming biomarkers and details, wherever appropriate, clinical use and differential diagnostics aspects.
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| 39. |
- Zetterberg, Henrik, 1973, et al.
(författare)
-
Chronic traumatic encephalopathy: fluid biomarkers.
- 2018
-
Ingår i: Handbook of clinical neurology. - 0072-9752. ; 158, s. 323-333
-
Tidskriftsartikel (refereegranskat)abstract
- Chronic traumatic encephalopathy (CTE) is a neuropathologic condition that has been described in individuals who have been exposed to repetitive head impacts, including concussions and subconcussive trauma. CTE cannot currently be diagnosed during life. Clinical symptoms of CTE (including changes in mood, behavior, and cognition) are nonspecific and may develop after a latency phase following the injuries. Differential diagnosis based solely on clinical features is, therefore, difficult. For example, some younger patients who do not experience the latency phase (i.e., symptoms of CTE may begin while still being exposed to the repetitive head impacts) may be clinically diagnosed with postconcussive syndrome, a vaguely defined condition that is described in a minority of concussed patients. Some older patients whose initial features of CTE include memory and executive dysfunction and progress to impaired activities of daily living may be clinically diagnosed with Alzheimer disease or another dementia. Although concussions are common in athletes and nonathletes, contact/collision sport athletes, such as boxers, American football players, and ice hockey players, are at greater risk of exposure to both concussion and repetitive subconcussive head impacts. Biomarkers for CTE pathophysiology would be of great value to study and improve our understanding of when and how the disease process starts and develops, as well as how it can be prevented or treated. Here, we review the literature regarding fluid biomarkers for repetitive subconcussive impacts, concussion, postconcussive syndrome, and CTE. We also discuss technical issues and potential pathways forward regarding how to move the most promising biomarker candidates into clinical laboratory practice.
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