Aβ1-42

Previous studies provided that Aβ1-42 peptide, a pathological component of Alzheimer's disease (AD), and α-synuclein, the major protein of Lewy bodies in Parkinson's disease (PD), may interact with transcription factors and affect gene transcription. Researchers have revealed that Aβ1-42 can be found in the nucleus, interact with DNA, and change the expression of many genes. It is known that α-synuclein functions as a transcription factor that binds to nuclear DNA and modulates the expression of many genes. Our study aims to investigate whether these peptides directly affect the expression of

Immunotherapy of Alzheimer’s disease (AD) is a promising approach to reduce the accumulation of amyloid-beta (Aβ) peptides, a critical event in the onset of the disease. Emerging evidence indicate that metabotropic glutamate receptors (mGluRs) are involved in the progression of AD, representing potential targets for new treatments. Studies have highlighted the potential role of group II mGluRs, mGluR2 and mGluR3, in the modulation of Aβ production, although their respective contribution remains unclear, due to the lack of specific tools to study them. Here, we showed in vitro that enhancing mG

Achieving early diagnosis in Alzheimer's disease (AD) is a crucial objective in preclinical and clinical AD research, since it represents a therapeutic window during which interventions can be initiated before the onset of severe cognitive decline. Accumulation of amyloid-beta (Aß) in the prefrontal cortex is linked to rapid forgetting in this prodromal AD stage. Thus, early forgetting becomes a potential target for preclinical studies seeking to prevent/delay the onset of severe forms of AD. We used mouse models to identify early alterations in memory formation. Our findings indicate that Aβ1

Recent data propose that Alzheimer’s disease (AD) should be considered as a systemic disease with a strong immune component. However, direct targeting of the immune system contribution to AD has been so far minimally explored. Here, by using a systems biology approach based on network integration of text mining and genomic data, we identified glucose‐6‐phosphate dehydrogenase (G6PD) as a target that may modulate neutrophil function and, in turn, down-regulate the immune system related damage in AD. Pharmacological and siRNA modulation, performed in differentiated HL-60 cells and primary neutro

Oxidative stress and neuroinflammation are crucial phenomena in the pathogenesis of Alzheimer disease (AD). Oxotremorine-M (Oxo), a non-selective muscarinic acetylcholine receptors agonist, exerts neurotrophic functions in primary neurons and modulates oxidative stress and neuroinflammation phenomena in rat brain. Based on this, our study investigates Oxo positive effects on differentiated SH-SY5Y neuroblastoma cells, revealing that Oxo treatment a) enhances cell survival, b) increases neurite length and c) upregulates HSP70 and pHSF1 expression. Moreover, Oxo counteracts tert–Butyl hydroperox

Alzheimer's disease (AD) is the leading cause of dementia during aging. While its pathological hallmarks have been identified, disease-modifying treatments are not yet available. Therefore, there is increasing interest in studying lifestyle interventions that could help in the prevention and mitigation of the symptoms. In this context, we aim to study the effect of green exposure and particularly of phytochemicals inhalation, focusing on terpenes, specifically pinene, widespread in Italy. For this purpose, we set up two stem cell models of AD. The first is NE-4C, a murine neural stem cell line