Omega-3 Fatty Acids Increase Amyloid-β Immunity, Energy, and Circadian Rhythm for Cognitive Protection of Alzheimer's Disease Patients Beyond Cholinesterase Inhibitors.
Aged
Aged, 80 and over
Alzheimer Disease
/ diet therapy
Amyloid beta-Peptides
/ immunology
Cholinesterase Inhibitors
/ administration & dosage
Circadian Rhythm
/ drug effects
Dietary Supplements
Fatty Acids, Omega-3
/ administration & dosage
Female
Humans
Macrophages
/ drug effects
Male
Mental Status and Dementia Tests
Middle Aged
Phagocytosis
/ drug effects
Prospective Studies
Amyloid-beta
bioenergy
cell signaling
cholinesterase inhibitor
glycolysis
phagocytosis
tricarboxylic cycle
ω-3 fatty acids
Journal
Journal of Alzheimer's disease : JAD
ISSN: 1875-8908
Titre abrégé: J Alzheimers Dis
Pays: Netherlands
ID NLM: 9814863
Informations de publication
Date de publication:
2020
2020
Historique:
pubmed:
12
5
2020
medline:
11
5
2021
entrez:
12
5
2020
Statut:
ppublish
Résumé
The cholinesterase inhibitor therapeutics (CI) approved for use in Alzheimer's disease (AD) are palliative for a limited time. To examine the outcome of AD patients with add-on therapy of the omega-3 fatty acid drink Smartfish. We performed a prospective study using Mini-Mental State Examination, amyloid-β (Aβ) phagocytosis blood assay, and RNA-seq of peripheral blood mononuclear cells in 28 neurodegenerative patients who had failed their therapies, including 8 subjective cognitive impairment (SCI), 8 mild cognitive impairment (MCI), 2 AD dementia, 1 frontotemporal dementia (FTD), 2 vascular cognitive impairment, and 3 dementia with Lewy bodies (DLB) patients. MCI, FTD, and DLB patients patients volunteered for the addition of a ω-3 fatty acid drink Smartfish protected by anti-oxidants to failing CI therapy. On this therapy, all MCI patients improved in the first year energy transcripts, Aβ phagocytosis, cognition, and activities of daily living; in the long term, they remained in MCI status two to 4.5 years. All FTD and DLB patients rapidly progressed to dementia. On in vivo or in vitroω-3 treatments, peripheral blood mononuclear cells of MCI patients upregulated energy enzymes for glycolysis and citric acid cycle, as well as the anti-inflammatory circadian genes CLOCK and ARNTL2. Add-on ω-3 therapy to CI may delay dementia in certain patients who had failed single CI therapy.
Sections du résumé
BACKGROUND
The cholinesterase inhibitor therapeutics (CI) approved for use in Alzheimer's disease (AD) are palliative for a limited time.
OBJECTIVE
To examine the outcome of AD patients with add-on therapy of the omega-3 fatty acid drink Smartfish.
METHODS
We performed a prospective study using Mini-Mental State Examination, amyloid-β (Aβ) phagocytosis blood assay, and RNA-seq of peripheral blood mononuclear cells in 28 neurodegenerative patients who had failed their therapies, including 8 subjective cognitive impairment (SCI), 8 mild cognitive impairment (MCI), 2 AD dementia, 1 frontotemporal dementia (FTD), 2 vascular cognitive impairment, and 3 dementia with Lewy bodies (DLB) patients.
RESULTS
MCI, FTD, and DLB patients patients volunteered for the addition of a ω-3 fatty acid drink Smartfish protected by anti-oxidants to failing CI therapy. On this therapy, all MCI patients improved in the first year energy transcripts, Aβ phagocytosis, cognition, and activities of daily living; in the long term, they remained in MCI status two to 4.5 years. All FTD and DLB patients rapidly progressed to dementia. On in vivo or in vitroω-3 treatments, peripheral blood mononuclear cells of MCI patients upregulated energy enzymes for glycolysis and citric acid cycle, as well as the anti-inflammatory circadian genes CLOCK and ARNTL2.
CONCLUSION
Add-on ω-3 therapy to CI may delay dementia in certain patients who had failed single CI therapy.
Identifiants
pubmed: 32390637
pii: JAD200252
doi: 10.3233/JAD-200252
pmc: PMC10190202
mid: NIHMS1891630
doi:
Substances chimiques
Amyloid beta-Peptides
0
Cholinesterase Inhibitors
0
Fatty Acids, Omega-3
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
993-1002Subventions
Organisme : NINDS NIH HHS
ID : R01 NS078410
Pays : United States
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