Thermoregulation in amyotrophic lateral sclerosis
(2018) In Handbook of Clinical Neurology 157. p.749-760- 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... (More)
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.
(Less)
- author
- Dupuis, Luc ; Petersen, Åsa LU and Weydt, Patrick
- organization
- publishing date
- 2018
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- keywords
- amyotrophic lateral sclerosis, body temperature, brown adipose tissue, dynein, energy homeostasis, frontotemporal dementia, PGC-1α, skeletal muscle, SOD1, sympathetic nervous system, TDP-43
- host publication
- Handbook of Clinical Neurology
- series title
- Handbook of Clinical Neurology
- volume
- 157
- pages
- 12 pages
- publisher
- Elsevier
- external identifiers
-
- scopus:85056629742
- pmid:30459038
- ISSN
- 2212-4152
- 0072-9752
- DOI
- 10.1016/B978-0-444-64074-1.00046-X
- language
- English
- LU publication?
- yes
- id
- d623991f-3142-41a0-8f3e-b0c6e096a78b
- date added to LUP
- 2018-11-28 13:33:31
- date last changed
- 2024-04-01 16:26:22
@inbook{d623991f-3142-41a0-8f3e-b0c6e096a78b,
abstract = {{<p>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.</p>}},
author = {{Dupuis, Luc and Petersen, Åsa and Weydt, Patrick}},
booktitle = {{Handbook of Clinical Neurology}},
issn = {{2212-4152}},
keywords = {{amyotrophic lateral sclerosis; body temperature; brown adipose tissue; dynein; energy homeostasis; frontotemporal dementia; PGC-1α; skeletal muscle; SOD1; sympathetic nervous system; TDP-43}},
language = {{eng}},
pages = {{749--760}},
publisher = {{Elsevier}},
series = {{Handbook of Clinical Neurology}},
title = {{Thermoregulation in amyotrophic lateral sclerosis}},
url = {{http://dx.doi.org/10.1016/B978-0-444-64074-1.00046-X}},
doi = {{10.1016/B978-0-444-64074-1.00046-X}},
volume = {{157}},
year = {{2018}},
}