1. Amnestic mild cognitive impairment and conversion to Alzheimer's disease: insulin resistance and glycoxidation as early biomarker clusters.

    Journal of Alzheimer's Disease 45(1):89 (2015) PMID 25471189

    Autopsy studies have indicated brain accumulation of amyloid-β peptides as a common pathogenetic hallmark of amnestic cognitive impairment (aMCI) and overt Alzheimer's disease (AD). The pathogenesis of AD is still debated but recent reports have even designated AD as type III diabetes. This stud...
  2. Aβ1-42 monomers or oligomers have different effects on autophagy and apoptosis.

    Autophagy 10(10):1827 (2014) PMID 25136804 PMCID PMC4198366

    The role of autophagy and its relationship with apoptosis in Alzheimer disease (AD) pathogenesis is poorly understood. Disruption of autophagy leads to buildup of incompletely digested substrates, amyloid-β (Aβ) peptide accumulation in vacuoles and cell death. Aβ, in turn, has been found to affe...
  3. Monomeric Aβ1–42 and RAGE: key players in neuronal differentiation

    Neurobiology of Aging 35(6):1301 (2014)

    The aggregation of amyloid-β (Aβ) peptides plays a crucial role in the onset and progression of Alzheimer's disease. Monomeric form of Aβ, indeed, could exert a physiological role. Considering the anti-oligomerization property of all-trans retinoic acid (ATRA), the involvement of monom...
  4. Monomeric Aβ1-42 and RAGE: key players in neuronal differentiation.

    Neurobiology of Aging 35(6):1301 (2014) PMID 24484607

    The aggregation of amyloid-β (Aβ) peptides plays a crucial role in the onset and progression of Alzheimer's disease. Monomeric form of Aβ, indeed, could exert a physiological role. Considering the anti-oligomerization property of all-trans retinoic acid (ATRA), the involvement of monomeric Aβ1-4...
  5. Adjunctive agomelatine therapy in the treatment of acute bipolar II depression: a preliminary open label study.

    Neuropsychiatric Disease and Treatment 9:243 (2013) PMID 23430979 PMCID PMC3575211

    The circadian rhythm hypothesis of bipolar disorder (BD) suggests a role for melatonin in regulating mood, thus extending the interest toward the melatonergic antidepressant agomelatine as well as type I (acute) or II cases of bipolar depression. Twenty-eight depressed BD-II patients received op...
  6. Survival rate in patients affected by dementia followed by memory clinics (UVA) in Italy.

    Journal of Alzheimer's Disease 36(2):303 (2013) PMID 23609761

    People affected by dementia experienced decreased life expectancy with a 2-4 times higher risk of death at a given age compared to non-demented people. Dementia represents a major cost to health care and society in the Western world and, particularly in Italy, is projected to become a high-resou...
  7. Aβ1-42-mediated down-regulation of Uch-L1 is dependent on NF-κB activation and impaired BACE1 lysosomal degradation.

    Aging Cell 11(5):834 (2012) PMID 22726800

    Amyloid-β 1-42 accumulation is the major pathogenetic event in Alzheimer's disease (AD), believed to be responsible for synaptic dysfunction and neuronal cell death. However, the physiologic activity of Aβ peptides remains elusive: Aβ might not only play a toxic role, but also act as a functiona...
  8. Amyloid-β production: major link between oxidative stress and BACE1.

    Neurotoxicity Research 22(3):208 (2012) PMID 22002808

    Sequential endoproteolytic cleavages operated by the γ-secretase and the β-secretase (BACE1) on the β-amyloid precursor protein result in the production of the β-amyloid (Aβ) species, with two C-terminal variants, at residue 40 or at residue 42. Accumulation in brain tissue of aggregates of Aβ42...
  9. β-amyloid 1-42 induces physiological transcriptional regulation of BACE1.

    Journal of Neurochemistry 122(5):1023 (2012) PMID 22708832

    The pathogenesis of Alzheimer's disease (AD) is only partially understood. β-amyloid (Aβ) is physiologically generated by sequential cleavage of its precursor protein by the β- and the γ-secretase and it is normally disposed of. In Alzheimer's disease, Aβ is excessively produced or less dismisse...
  10. The earliest stage of cognitive impairment in transition from normal aging to Alzheimer disease is marked by prominent RNA oxidation in vulnerable neurons.

    Journal of Neuropathology & Experimental Neurology 71(3):233 (2012) PMID 22318126 PMCID PMC3288284

    Although neuronal RNA oxidation is a prominent and established feature in age-associated neurodegenerative disorders such as Alzheimer disease (AD), oxidative damage to neuronal RNA in aging and in the transitional stages from normal elderly to the onset of AD has not been fully examined. In thi...
  11. Position paper of the Italian Society for the study of Dementias (SINDEM) on the proposal of a new lexicon on Alzheimer disease.

    Neurological Sciences 33(1):201 (2012) PMID 22057264

    A panel of Italian neurologists of the Italian Society for the study of Dementias (SINDEM) discussed the recently proposed new lexicon for Alzheimer disease (AD) and the related diagnostic criteria for the different phases of the disease (Preclinical AD, prodromal AD and Alzheimer's dementia) (D...
  12. AGEs/RAGE complex upregulates BACE1 via NF-κB pathway activation

    Neurobiology of Aging 33(1):196.e13 (2012)

    Although the pathogenesis of sporadic Alzheimer disease (AD) is not clearly understood, it is likely dependent on several age-related factors. Diabetes is a risk factor for AD, and multiple mechanisms connecting the 2 diseases have been proposed. Hyperglycemia enhances the formation of adva...
  13. Possible influence of a non-synonymous polymorphism located in the NGF precursor on susceptibility to late-onset Alzheimer's disease and mild cognitive impairment.

    Journal of Alzheimer's Disease 29(3):699 (2012) PMID 22330829

    The complex network of neurotrophic factors is supposed to play a role in neurodegeneration, but the effect of variations in their coding genes on susceptibility to sporadic Alzheimer's disease is not established. The mature form of nerve growth factor (NGF) derives from a precursor, proNGF, whi...
  14. AGEs/RAGE complex upregulates BACE1 via NF-κB pathway activation.

    Neurobiology of Aging 33(1):196.e13 (2012) PMID 20638753

    Although the pathogenesis of sporadic Alzheimer disease (AD) is not clearly understood, it is likely dependent on several age-related factors. Diabetes is a risk factor for AD, and multiple mechanisms connecting the 2 diseases have been proposed. Hyperglycemia enhances the formation of advanced ...
  15. A novel origin for granulovacuolar degeneration in aging and Alzheimer's disease: parallels to stress granules.

    Laboratory Investigation 91(12):1777 (2011) PMID 21968813 PMCID PMC3428037

    The phosphorylated ribosomal protein S6 (pS6) is associated with the 40S ribosomal subunit in eukaryotes and is thought to have a role in RNA storage, degradation, and re-entry into translation. In this study, we found pS6 localized to granulovacuolar degeneration (GVD) within the pyramidal neur...
  16. The cell cycle regulator phosphorylated retinoblastoma protein is associated with tau pathology in several tauopathies.

    Journal of Neuropathology & Experimental Neurology 70(7):578 (2011) PMID 21666500 PMCID PMC3122485

    Retinoblastoma protein (pRb) is a ubiquitous 928-amino acid cell cycle regulatory molecule with diverse biologic activities. One critical function of pRb is the control of the G1-to-S phase checkpoint of the cell cycle. In the hypophosphorylated state, pRb suppresses the activity of E2F transcri...
  17. RNA polymerase III drives alternative splicing of the potassium channel-interacting protein contributing to brain complexity and neurodegeneration.

    Journal of Cell Biology 193(5):851 (2011) PMID 21624954 PMCID PMC3105541

    Alternative splicing generates protein isoforms that are conditionally or differentially expressed in specific tissues. The discovery of factors that control alternative splicing might clarify the molecular basis of biological and pathological processes. We found that IL1-α-dependent up-regulati...
  18. 17A, a novel non-coding RNA, regulates GABA B alternative splicing and signaling in response to inflammatory stimuli and in Alzheimer disease.

    Neurobiology of Disease 41(2):308 (2011) PMID 20888417

    Alternative splicing is a central component of human brain complexity; nonetheless, its regulatory mechanisms are still largely unclear. In this work, we describe a novel non-coding (nc) RNA (named 17A) RNA polymerase (pol) III-dependent embedded in the human G-protein-coupled receptor 51 gene (...
  19. 17A, a novel non-coding RNA, regulates GABA B alternative splicing and signaling in response to inflammatory stimuli and in Alzheimer disease

    Neurobiology of Disease 41(2):308 (2011)

    Alternative splicing is a central component of human brain complexity; nonetheless, its regulatory mechanisms are still largely unclear. In this work, we describe a novel non-coding (nc) RNA (named 17A) RNA polymerase (pol) III-dependent embedded in the human G-protein-coupled receptor 51 g...
  20. Amyloid-β₄₂ activates the expression of BACE1 through the JNK pathway.

    Journal of Alzheimer's Disease 27(4):871 (2011) PMID 21897006

    The sequential endoproteolytic cleavages operated by the γ-secretase and the β-secretase (BACE1) on the amyloid-β protein precursor (AβPP) result in the production of the amyloid-β (Aβ) species, with two C-terminal variants, at residue 40 or at residue 42. Accumulation in brain tissue of small, ...