Interplay between Aβ, Ceramides and Hyperphosphorylated Tau in Alzheimer’s Disease (CROSBI ID 54445)
Prilog u knjizi | izvorni znanstveni rad
Podaci o odgovornosti
Jazvinšćak Jembrek, Maja ; Babić, Mirjana ; Pivac, Nela ; Šimić, Goran
engleski
Interplay between Aβ, Ceramides and Hyperphosphorylated Tau in Alzheimer’s Disease
Alzheimer's disease (AD), the most common leading form of dementia in elderly people, is a chronic and progressive neurodegenerative disorder. The most frequently investigated neuropathological hallmarks of AD are extracellular deposits of neurotoxic amyloid β peptide (Aβ) and intracellular aggregates of hyperphosphorylated tau protein. Ceramides, the major molecules of sphingolipid metabolism, have been linked to AD susceptibility and pathogenesis, including both Aβ pathology and tau aggregation. Elevated levels of ceramides directly increase Aβ levels acting on β- secretase, a key enzyme in the proteolytic cleavage of Aβ precursor protein (APP). In turn, soluble and fibrillar forms of Aβ activate sphingomyelinases, enzymes that catalyze the breakdown of sphingomyelin to ceramides, and lead to further increase in Aβ generation. Ceramides are also linked to tau phosphorylation, in particular by modulating activity of protein phosphatase 2A, the major tau phosphatase in the human brain. Hence, preservation of neuronal ceramide homeostasis is of major importance for normal brain functioning. This chapter summarizes recent findings and potential targets for novel therapeutic approaches in AD regarding described devastating Aβ-ceramides-tau cascade.
Ceramides, Aβ, Phospho-tau, Alzheimer's disease
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Podaci o prilogu
53-84.
objavljeno
Podaci o knjizi
Sphingomyelin and Ceramides: Occurrence, Biosynthesis and Role in Disease
Watkins, Cecilia L.
New York (NY): Nova Science Publishers
2015.
978-1-63482-553-5