Sulforaphane Upregulates the Heat Shock Protein Co-Chaperone CHIP and Clears Amyloid-β and Tau in a Mouse Model of Alzheimer's Disease.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and in vitro laboratory study
PubMed 29714053 · doi:10.1002/mnfr.201800240
What was done
The authors evaluated the therapeutic effects of sulforaphane, an isothiocyanate from cruciferous vegetables, in a triple transgenic mouse model of Alzheimer's disease (3×Tg-AD) and in CHIP-deficient primary neurons derived from these mice. Mice received oral gavage of sulforaphane. Investigators assessed protein and mRNA levels of amyloid-β (Aβ), tau, phosphorylated tau, amyloid precursor protein (APP), heat shock protein 70 (HSP70), and the co-chaperone C-terminus of HSP70-interacting protein (CHIP). Cognitive performance was measured using novel object/location recognition tests and contextual fear conditioning assays.
What was found
The abstract reports qualitative directions of effect without reporting quantitative values: - Sulforaphane oral gavage reduced protein levels of monomeric and polymeric Aβ, total tau, and phosphorylated tau without altering mRNA expression of APP or tau. - Sulforaphane increased protein levels of CHIP and HSP70. - In primary neurons, sulforaphane increased CHIP expression and cleared Aβ and tau accumulation. - Sulforaphane administration improved memory deficits in behavioral tests (novel object/location recognition and contextual fear conditioning).
Why it matters
The study identifies a potential mechanism whereby sulforaphane promotes the clearance of pathological Aβ and tau aggregates via upregulation of the HSP70 co-chaperone CHIP, offering a preclinical rationale for exploring dietary isothiocyanates in neurodegenerative proteinopathies.
Limits
This was strictly an animal (3×Tg-AD mice) and cell-culture study; findings cannot be directly translated to human Alzheimer's disease pathology or clinical outcomes. The abstract does not report sample sizes, specific dosages, treatment durations, or quantitative data (such as exact percentage reductions or confidence intervals). Bioavailability, blood-brain barrier penetration in humans, and potential toxicities were not described in the abstract.
Cited by
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