Abstract
Several therapies for Alzheimer's Disease (AD) are currently under investigation. Some studies have reported that concentration of vitamins in biological fluids are lower in AD patients compared to control subjects and clinical evidence has shown the therapeutic potential of vitamin C and E in delaying AD progression. However, the molecular mechanism(s) that are engaged upon their administration in the APP metabolism in vitro or in vivo still need clarifying. Here, we investigate the effects of vitamin C supplementation, at physiological concentration, in skin fibroblasts obtained from SAD and FAD patients. This study shows that SAD patients' fibroblasts exhibited the exclusive appearance of C-terminal fragments, derived from APP processing, without giving rise to the β-amyloid peptide, other than corresponding decreased levels of lysosomal enzymes, such as β-hexosaminidase, α-mannosidase and cathepsins B, L, and D.
| Original language | English |
|---|---|
| Pages (from-to) | 2510-2515 |
| Number of pages | 6 |
| Journal | Neurochemical Research |
| Volume | 33 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - Dec 2008 |
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Keywords
- β-Amyloidogenesis
- Alzheimer's disease
- Experimental model for AD
- Lysosomal enzymes
- Skin fibroblasts
- Vitamin C
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Biochemistry
Cite this
Effects of vitamin C on fibroblasts from sporadic Alzheimer's disease patients. / Costanzi, Egidia; Martino, Sabata; Persichetti, Emanuele; Tiribuzi, Roberto; Massini, Carlo; Bernardi, Giorgio; Orlacchio, Antonio; Orlacchio, Aldo.
In: Neurochemical Research, Vol. 33, No. 12, 12.2008, p. 2510-2515.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of vitamin C on fibroblasts from sporadic Alzheimer's disease patients
AU - Costanzi, Egidia
AU - Martino, Sabata
AU - Persichetti, Emanuele
AU - Tiribuzi, Roberto
AU - Massini, Carlo
AU - Bernardi, Giorgio
AU - Orlacchio, Antonio
AU - Orlacchio, Aldo
PY - 2008/12
Y1 - 2008/12
N2 - Several therapies for Alzheimer's Disease (AD) are currently under investigation. Some studies have reported that concentration of vitamins in biological fluids are lower in AD patients compared to control subjects and clinical evidence has shown the therapeutic potential of vitamin C and E in delaying AD progression. However, the molecular mechanism(s) that are engaged upon their administration in the APP metabolism in vitro or in vivo still need clarifying. Here, we investigate the effects of vitamin C supplementation, at physiological concentration, in skin fibroblasts obtained from SAD and FAD patients. This study shows that SAD patients' fibroblasts exhibited the exclusive appearance of C-terminal fragments, derived from APP processing, without giving rise to the β-amyloid peptide, other than corresponding decreased levels of lysosomal enzymes, such as β-hexosaminidase, α-mannosidase and cathepsins B, L, and D.
AB - Several therapies for Alzheimer's Disease (AD) are currently under investigation. Some studies have reported that concentration of vitamins in biological fluids are lower in AD patients compared to control subjects and clinical evidence has shown the therapeutic potential of vitamin C and E in delaying AD progression. However, the molecular mechanism(s) that are engaged upon their administration in the APP metabolism in vitro or in vivo still need clarifying. Here, we investigate the effects of vitamin C supplementation, at physiological concentration, in skin fibroblasts obtained from SAD and FAD patients. This study shows that SAD patients' fibroblasts exhibited the exclusive appearance of C-terminal fragments, derived from APP processing, without giving rise to the β-amyloid peptide, other than corresponding decreased levels of lysosomal enzymes, such as β-hexosaminidase, α-mannosidase and cathepsins B, L, and D.
KW - β-Amyloidogenesis
KW - Alzheimer's disease
KW - Experimental model for AD
KW - Lysosomal enzymes
KW - Skin fibroblasts
KW - Vitamin C
UR - http://www.scopus.com/inward/record.url?scp=56349156021&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=56349156021&partnerID=8YFLogxK
U2 - 10.1007/s11064-007-9539-y
DO - 10.1007/s11064-007-9539-y
M3 - Article
C2 - 18046644
AN - SCOPUS:56349156021
VL - 33
SP - 2510
EP - 2515
JO - Neurochemical Research
JF - Neurochemical Research
SN - 0364-3190
IS - 12
ER -