Smoking-associated protection from Alzheimer's and Parkinson's disease

Morens, DavidM.; Grandinetti, Andrew; Reed, Dwayne; White, LonR.

doi:10.1016/s0140-6736(94)91194-0

Cited by 19 publications

(8 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that nicotine exerts broad effects on the CNS, such as memory improvement (Rezvani and Levin 2001), release of neurotransmitters (Okuda et al 1994; Serova and Sabban 2002) and neurotrophic factors (Belluardo et al 2004), and protection of neurons from apoptosis (Garrido et al 2001; Guan et al 2003; Hejmadi et al 2003). For example, cigarette smoking has a protective effect against AD and PD (Fratiglioni and Wang 2000; Morens et al 1994) by affecting cellular inflammation. Further, improved cognitive performance has been identified in healthy non-smokers and AD patients after a short period of nicotine treatment.…”

Section: Discussionmentioning

confidence: 99%

Modulation of innate immune-related pathways in nicotine-treated SH-SY5Y cells

et al. 2011

View full text Add to dashboard Cite

Although nicotine has a broad impact on both the central and peripheral nervous systems, the molecular mechanisms remain largely unknown, especially at the signaling pathway level. To investigate that aspect, we employed both conventional molecular techniques, such as quantitative real-time PCR and Western blotting analysis, and high-throughput microarray approach to identify the genes and signaling pathways that are modulated by nicotine. We found 14 pathways significantly altered in SH-SY5Y neuroblastoma cells. Of these, the Toll-like receptor pathway (TLR; p = 2.57 × 10−4) is one of the most important innate immune pathways. The death receptor pathway (DR; p = 8.71 × 10−4), whose transducers coordinate TLR signals and help conduct the host immune response to infection, was also significantly changed by nicotine. Furthermore, we found that several downstream pathways of TLR and DR signaling, such as PI3K/AKT signaling (p = 9.55 × 10−6), p38 signaling (p = 2.40 × 10−6), and ERK signaling (p = 1.70 × 10−4), were also significantly modulated by nicotine. Interestingly, most of the differentially expressed genes in these pathways leading to nuclear factor κB (NF-κB) activation and those important inhibitors of pathways leading to apoptosis, including FLIP and Bcl-2, were up-regulated by nicotine. Taken together, our findings demonstrate that nicotine can regulate multiple innate immune-related pathways, and our data thus provide new clues to the molecular mechanisms underlying nicotine's regulatory effects on neurons.

show abstract

Section: Discussionmentioning

confidence: 99%

Modulation of innate immune-related pathways in nicotine-treated SH-SY5Y cells

et al. 2011

View full text Add to dashboard Cite

show abstract

“…There is a fascinating apparent inverse relationship between smoking and the risk for PD (Morens et al 1994 ;Rybicki et al 1999). Two explanations have been offered for this observation.…”

Section:   mentioning

confidence: 99%

Genetics of Parkinsonism: a review

VAUGHAN¹,

DAVIS²,

WOOD³

2001

Annals of Human Genetics

View full text Add to dashboard Cite

Idiopathic Parkinson's disease (IPD), a progressive neurodegenerative disorder, is a common cause of disability. No current therapies modify disease progression. The pathological hallmarks are the presence of Lewy bodies and massive loss of dopaminergic neurons in the pars compacta of the substantia nigra. Two genes (SNCA and parkin) as well as two gene loci have now been implicated in the pathogenesis of familial PD. These represent significant progress in our understanding of the disease, considering the rarity of large families, low heritability in the general population and genetic heterogeneity. Mutations in a further gene, UCHL1, have been described in familial PD although the evidence for its role in PD is less clear. Knowledge of the genes described in PD to date should help to define molecular mechanisms of neurodegeneration in PD, as well as in other diseases where defects in protein handling may be a common feature. Nigral degeneration with Lewy body formation and the resulting clinical picture of PD may represent a final common pathway of a multifactorial disease process in which both environmental and genetic factors have a role. This review discusses the major advances in the field to date and illustrates how the existence of genetic factors has now become firmly established.

show abstract

“…Because [3H]nicotinic acetylcholine binding has been consistently reported to be reduced in patients with AD compared to controls (40), a possible biologic mechanism may be the lack of or a decrease in the stimulating effect of nicotine on the central nervous system. There is an animated debate in the literature concerning the interpretation of these results and the possible protective effect of smoking in AD (41)(42)(43)(44)(45)(46). No definite conclusion can be drawn at the present time.…”

Section: Possible Risk Factorsmentioning

confidence: 99%

Epidemiology of Alzheimer's disease and current possibilities for prevention

Fratiglioni

1996

Acta Neurologica Scandinavica

View full text Add to dashboard Cite

Many epidemiological studies of Alzheimer's disease (AD) have been conducted. This review discusses the most recent findings in relation to the possibilities of prevention of this disease. Data on the diagnostic validity are also reported. The primary prevention of AD is hampered by limitations in the knowledge and understanding about its risk factors. Among the factors that have been investigated, only age, familial aggregation, and apolipoprotein E gene‐e4 allele are definite risk factors both for early‐ and late‐onset AD. However, many of the possible and putative risk factors, if definitely confirmed, can be prevented or controlled. Secondary prevention is not currently practicable as valid predictive tests and efficacious treatment are lacking. In contrast, much data is available to support tertiary prevention interventions, such as better planned patient care.

show abstract

Smoking-associated protection from Alzheimer's and Parkinson's disease

Cited by 19 publications

References 1 publication

Modulation of innate immune-related pathways in nicotine-treated SH-SY5Y cells

Modulation of innate immune-related pathways in nicotine-treated SH-SY5Y cells

Genetics of Parkinsonism: a review

Epidemiology of Alzheimer's disease and current possibilities for prevention

Contact Info

Product

Resources

About