Abstract
Alzheimer's disease is the most common form of dementia among older people and is still untreatable. While β-amyloid protein is recognized as the disease determinant with a pivotal role in inducing neuronal loss and dementia, an impaired brain insulin signaling seems to account in part for the cognitive deficit associated with the disease. The origin of this defective signaling is uncertain. Accumulating toxic species of β-amyloid, the so-called oligomers, has been proposed to be responsible for downregulation of neuronal insulin receptors. We have found that the nontoxic form of β-amyloid, the monomer, is able to activate insulin/insulin-like growth factor-1 (IGF-1) receptor signaling and thus behaves as a neuroprotectant agent. Our suggestion is that depletion of β-amyloid monomers, occurring in the preclinical phase of Alzheimer's disease, might be the cause of early insulin/IGF-1 signaling disturbances that anticipate cognitive decline.
| Original language | English |
|---|---|
| Pages (from-to) | 605-613 |
| Number of pages | 9 |
| Journal | Molecular Neurobiology |
| Volume | 46 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2012 |
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Keywords
- β-Amyloid
- Alzheimer's disease
- Insulin
- Insulin-like growth factor 1
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
Cite this
Beta-Amyloid monomer and insulin/IGF-1 signaling in Alzheimer's disease. / Giuffrida, Maria Laura; Tomasello, Flora; Caraci, Filippo; Chiechio, Santina; Nicoletti, Ferdinando; Copani, Agata.
In: Molecular Neurobiology, Vol. 46, No. 3, 2012, p. 605-613.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Beta-Amyloid monomer and insulin/IGF-1 signaling in Alzheimer's disease
AU - Giuffrida, Maria Laura
AU - Tomasello, Flora
AU - Caraci, Filippo
AU - Chiechio, Santina
AU - Nicoletti, Ferdinando
AU - Copani, Agata
PY - 2012
Y1 - 2012
N2 - Alzheimer's disease is the most common form of dementia among older people and is still untreatable. While β-amyloid protein is recognized as the disease determinant with a pivotal role in inducing neuronal loss and dementia, an impaired brain insulin signaling seems to account in part for the cognitive deficit associated with the disease. The origin of this defective signaling is uncertain. Accumulating toxic species of β-amyloid, the so-called oligomers, has been proposed to be responsible for downregulation of neuronal insulin receptors. We have found that the nontoxic form of β-amyloid, the monomer, is able to activate insulin/insulin-like growth factor-1 (IGF-1) receptor signaling and thus behaves as a neuroprotectant agent. Our suggestion is that depletion of β-amyloid monomers, occurring in the preclinical phase of Alzheimer's disease, might be the cause of early insulin/IGF-1 signaling disturbances that anticipate cognitive decline.
AB - Alzheimer's disease is the most common form of dementia among older people and is still untreatable. While β-amyloid protein is recognized as the disease determinant with a pivotal role in inducing neuronal loss and dementia, an impaired brain insulin signaling seems to account in part for the cognitive deficit associated with the disease. The origin of this defective signaling is uncertain. Accumulating toxic species of β-amyloid, the so-called oligomers, has been proposed to be responsible for downregulation of neuronal insulin receptors. We have found that the nontoxic form of β-amyloid, the monomer, is able to activate insulin/insulin-like growth factor-1 (IGF-1) receptor signaling and thus behaves as a neuroprotectant agent. Our suggestion is that depletion of β-amyloid monomers, occurring in the preclinical phase of Alzheimer's disease, might be the cause of early insulin/IGF-1 signaling disturbances that anticipate cognitive decline.
KW - β-Amyloid
KW - Alzheimer's disease
KW - Insulin
KW - Insulin-like growth factor 1
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U2 - 10.1007/s12035-012-8313-6
DO - 10.1007/s12035-012-8313-6
M3 - Article
C2 - 22886436
AN - SCOPUS:84880726942
VL - 46
SP - 605
EP - 613
JO - Molecular Neurobiology
JF - Molecular Neurobiology
SN - 0893-7648
IS - 3
ER -