Articles producció científica> Bioquímica i Biotecnologia

Long-term exposition to a high fat diet favors the appearance of β-amyloid depositions in the brain of C57BL/6J mice. A potential model of sporadic Alzheimer's disease

  • Identification data

    Identifier: imarina:5131076
    Authors:
    Busquets, OriolEttcheto, MirenPallas, MerceBeas-Zarate, CarlosVerdaguer, EsterAuladell, CarmeFolch, JaumeCamins, Antoni
    Abstract:
    AIMS: The sporadic and late-onset form of Alzheimer's disease (AD) constitutes the most common form of dementia. This non-familiar form could be a consequence of metabolic syndrome, characterized by obesity and the development of a brain-specific insulin resistance known as type III diabetes. This work demonstrates the development of a significant AD-like neuropathology due to these metabolic alterations. METHODS: C57BL/6J mice strain were divided into two groups, one fed with a diet rich in palmitic acid (high-fat diet, HFD) since their weaning until 16 months of age, and another group used as a control with a regular diet. The analyses were carried out in the dentate gyrus area of the hippocampus using a Thioflavin-S stain and immunofluorescence assays. RESULTS: The most significant finding of the present research was that HFD induced the deposition of the βA peptide. Moreover, the diet also caused alterations in different cell processes, such as increased inflammatory reactions that lead to a decrease in the neuronal precursor cells. In addition, the results show that there were also dysregulations in normal autophagy and apoptosis, mechanisms related to βA formation. CONCLUSIONS: The present findings confirm that HFD favors the formation of βA depositions in the brain, a key feature of AD, supporting the metabolic hypothesis of sporadic AD.
  • Others:

    Author, as appears in the article.: Busquets, Oriol; Ettcheto, Miren; Pallas, Merce; Beas-Zarate, Carlos; Verdaguer, Ester; Auladell, Carme; Folch, Jaume; Camins, Antoni
    Department: Bioquímica i Biotecnologia
    URV's Author/s: Folch Lopez, Jaume
    Keywords: Β-amyloid Up-regulation Type 2 diabetes mellitus T2dm, type 2 diabetes mellitus T2dm Ptp1β Ptp1? Ptp1 beta, protein tyrosine phosphatase 1 beta Protein tyrosine phosphatase 1β Protein tyrosine phosphatase 1? Obesity Mitogen-activated protein kinase Mice Metabolic syndrome Mechanisms Mapk, mitogen-activated protein kinase Mapk Load, late-onset alzheimer's disease Load Late-onset alzheimer’s disease Late-onset alzheimer's disease Jnk Insulin-like growth factor-1 Inflammation Igf-1, insulin-like growth factor-1 Igf-1 Humans High-fat diet High calorie diet Hfd, high-fat diet Hfd Hcd, high calorie diet Hcd Expression Energy metabolism Disease models, animal Dio, diet-induced obesity Dio Dietary fats Diet-induced obesity Csf, cerebrospinal fluid Csf Cerebrospinal fluid Brain blood barrier Brain Beta-site app-cleaving enzyme 1 Bbb, brain blood barrier Bbb Bace1, beta-site app-cleaving enzyme 1 Bace1 Aβ Autophagy Autonomic nervous system Ans. autonomic nervous system Ans Animals Amyloid beta-peptides Amyloid beta protein Ampk Ampik amp-activated protein kinase Amp-activated protein kinase Alzheimer’s disease Alzheimer's disease Alzheimer disease Aging Ad, alzheimer's disease Ad A? A beta, beta-amyloid ?-amyloid type 2 diabetes mellitus t2dm ptp1? protein tyrosine phosphatase 1? mitogen-activated protein kinase mapk load late-onset alzheimer’s disease insulin-like growth factor-1 igf-1 high-fat diet high calorie diet hfd hcd dio diet-induced obesity csf cerebrospinal fluid brain blood barrier beta-site app-cleaving enzyme 1 bbb bace1 autonomic nervous system ans ampk amp-activated protein kinase alzheimer’s disease ad a?
    Abstract: AIMS: The sporadic and late-onset form of Alzheimer's disease (AD) constitutes the most common form of dementia. This non-familiar form could be a consequence of metabolic syndrome, characterized by obesity and the development of a brain-specific insulin resistance known as type III diabetes. This work demonstrates the development of a significant AD-like neuropathology due to these metabolic alterations. METHODS: C57BL/6J mice strain were divided into two groups, one fed with a diet rich in palmitic acid (high-fat diet, HFD) since their weaning until 16 months of age, and another group used as a control with a regular diet. The analyses were carried out in the dentate gyrus area of the hippocampus using a Thioflavin-S stain and immunofluorescence assays. RESULTS: The most significant finding of the present research was that HFD induced the deposition of the βA peptide. Moreover, the diet also caused alterations in different cell processes, such as increased inflammatory reactions that lead to a decrease in the neuronal precursor cells. In addition, the results show that there were also dysregulations in normal autophagy and apoptosis, mechanisms related to βA formation. CONCLUSIONS: The present findings confirm that HFD favors the formation of βA depositions in the brain, a key feature of AD, supporting the metabolic hypothesis of sporadic AD.
    Thematic Areas: Medicina iii Medicina ii Medicina i Interdisciplinar Geriatrics & gerontology Educação física Developmental biology Ciências biológicas iii Ciências biológicas ii Ciências biológicas i Cell biology Biotecnología Biochemistry & molecular biology Aging
    licence for use: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 00476374
    Author's mail: jaume.folch@urv.cat
    Author identifier: 0000-0002-5051-8858
    Record's date: 2024-10-19
    Papper version: info:eu-repo/semantics/acceptedVersion
    Link to the original source: https://www.sciencedirect.com/science/article/abs/pii/S0047637416300859?via%3Dihub
    Licence document URL: https://repositori.urv.cat/ca/proteccio-de-dades/
    Papper original source: Mechanisms Of Ageing And Development. 162 38-45
    APA: Busquets, Oriol; Ettcheto, Miren; Pallas, Merce; Beas-Zarate, Carlos; Verdaguer, Ester; Auladell, Carme; Folch, Jaume; Camins, Antoni (2017). Long-term exposition to a high fat diet favors the appearance of β-amyloid depositions in the brain of C57BL/6J mice. A potential model of sporadic Alzheimer's disease. Mechanisms Of Ageing And Development, 162(), 38-45. DOI: 10.1016/j.mad.2016.11.002
    Article's DOI: 10.1016/j.mad.2016.11.002
    Entity: Universitat Rovira i Virgili
    Journal publication year: 2017
    Publication Type: Journal Publications
  • Keywords:

    Aging,Biochemistry & Molecular Biology,Cell Biology,Developmental Biology,Geriatrics & Gerontology
    Β-amyloid
    Up-regulation
    Type 2 diabetes mellitus
    T2dm, type 2 diabetes mellitus
    T2dm
    Ptp1β
    Ptp1?
    Ptp1 beta, protein tyrosine phosphatase 1 beta
    Protein tyrosine phosphatase 1β
    Protein tyrosine phosphatase 1?
    Obesity
    Mitogen-activated protein kinase
    Mice
    Metabolic syndrome
    Mechanisms
    Mapk, mitogen-activated protein kinase
    Mapk
    Load, late-onset alzheimer's disease
    Load
    Late-onset alzheimer’s disease
    Late-onset alzheimer's disease
    Jnk
    Insulin-like growth factor-1
    Inflammation
    Igf-1, insulin-like growth factor-1
    Igf-1
    Humans
    High-fat diet
    High calorie diet
    Hfd, high-fat diet
    Hfd
    Hcd, high calorie diet
    Hcd
    Expression
    Energy metabolism
    Disease models, animal
    Dio, diet-induced obesity
    Dio
    Dietary fats
    Diet-induced obesity
    Csf, cerebrospinal fluid
    Csf
    Cerebrospinal fluid
    Brain blood barrier
    Brain
    Beta-site app-cleaving enzyme 1
    Bbb, brain blood barrier
    Bbb
    Bace1, beta-site app-cleaving enzyme 1
    Bace1
    Autophagy
    Autonomic nervous system
    Ans. autonomic nervous system
    Ans
    Animals
    Amyloid beta-peptides
    Amyloid beta protein
    Ampk
    Ampik amp-activated protein kinase
    Amp-activated protein kinase
    Alzheimer’s disease
    Alzheimer's disease
    Alzheimer disease
    Aging
    Ad, alzheimer's disease
    Ad
    A?
    A beta, beta-amyloid
    ?-amyloid
    type 2 diabetes mellitus
    t2dm
    ptp1?
    protein tyrosine phosphatase 1?
    mitogen-activated protein kinase
    mapk
    load
    late-onset alzheimer’s disease
    insulin-like growth factor-1
    igf-1
    high-fat diet
    high calorie diet
    hfd
    hcd
    dio
    diet-induced obesity
    csf
    cerebrospinal fluid
    brain blood barrier
    beta-site app-cleaving enzyme 1
    bbb
    bace1
    autonomic nervous system
    ans
    ampk
    amp-activated protein kinase
    alzheimer’s disease
    ad
    a?
    Medicina iii
    Medicina ii
    Medicina
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