Apolipoprotein E Polymorphism and Alzheimer Disease

Ganguli, Mary; Chandra, Vijay; Kamboh, M. Ilyas; Johnston, Janet M.; Dodge, Hiroko H.; Thelma, B.K.; Juyal, Ramesh C.; Pandav, Rajesh; Belle, Steven H.; DeKosky, Steven T.

doi:10.1001/archneur.57.6.824

Cited by 296 publications

(167 citation statements)

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“…Data are presented as means ± SEM. * P<0.01 vs control (SHAM) and STZ-induced group, ANOVA followed by Tukey's test 2000) and the number of AD patients between 70 and 79 years of age living in India is approximately four times less than the population of people of the same age living in the United States (Ganguli et al 2000). In fact, accumulating cell culture and animal model data show that dietary CUR is a strong candidate for use in the prevention or treatment of major disabling agerelated neurodegenerative diseases (Cole et al 2007).…”

Section: Discussionmentioning

confidence: 96%

“…Aggregation of misfolded proteins that contain Aβ has been shown to initiate oxidative stress and inflammation and also to be responsible for the neurodegenerative changes and clinical properties of AD (Klein et al 2001). The ICV STZ model appears to produce cognitive deficits similar to those seen in SAD-type dementia (Hong and Lee 1997;Ganguli et al 2000;Salkovic-Petrisic and Hoyer 2007). The ICV STZ model mimics AD because of the cognitive impairment created by STZ.…”

Section: Discussionmentioning

confidence: 99%

“…The compound STZ is known to inhibit insulin receptor function, create persistent oxidative stress, mitochondrial dysfunction, impaired energy metabolism and activation of proapoptotic signalling pathways. All these effects of STZ are sufficient to mimic AD-type neurodegeneration (Hong and Lee 1997;Ganguli et al 2000;Salkovic-Petrisic and Hoyer 2007). Therefore, this study was undertaken to evaluate the effects of CUR on IGF-1, memory deficit and histopathological changes in the STZ-induced memory deficit model of SAD.…”

Section: Introductionmentioning

confidence: 99%

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Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

Işık

Çelik

Ulusoy

et al. 2008

AGE

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Increased serum insulin levels and reduced peripheral insulin activities seen in insulin resistance syndrome are associated with age-dependent cognitive impairment and Sporadic Alzheimer's Disease (SAD), suggesting a disturbance in the insulin signalling system in the brain and possibly being one of the causes of dementia. Therefore, the streptozotocin (STZ)-induced animal may be an appropriate model for the investigation of SAD and related dementia. This study was designed to investigate the beneficial effect of Curcumin (CUR), a neuroprotective agent, on intracerebroventricular (ICV) STZ-induced cognitive impairment in rats. For this purpose, adult male Wistar rats were bilaterally ICV injected with STZ (3 mg/kg). An artificial cerebrospinal fluid (aCSF) was given to the control group (SHAM) instead of STZ on days 1 and 3. Learning and memory performance were assessed using the "passive avoidance task" and the "Morris water maze test". After confirmation of acquisition impairment with these tests, the STZ group was divided into two subgroups: STZ+ vehicle (Vh) and STZ+CUR. The rats in the SHAM and STZ+Vh groups were administered intraperitoneally with 0.5 ml Vh and the rats in the STZ+CUR group were treated intraperitoneally with CUR (300 mg kg −1 day −1 in Vh) for 10 days starting from the 25th day after STZ injection. The Morris water maze test was reapplied on the 35th day after STZ injection and all of the rats were sacrificed on day 36 for quantitation of IGF-1 and for histopathological evaluation. Rats in the STZ+CUR group were found to have a higher performance in cognitive tests than rats in the STZ+Vh group (P<0.01). In parallel with the cognitive tests, IGF-1 levels were decreased in all of the STZ-injected groups (1.78±0.34) compared to the SHAM group (3.46±0.41). In contrast, CUR treatment significantly increased IGF-1 levels (P<0.001). The degree of neuronal loss decreased after CUR treatment compared to the SHAM group (P< 0.02). These results clearly indicate that CUR treatment is effective in reducing the cognitive impairment caused AGE

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

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Çelik

Ulusoy

et al. 2008

AGE

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“…Further research demonstrated that CTS improved the cognitive ability and promoted APP metabolism involving the non-amyloidogenic product pathway in rat cortical neuronal cells. Moreover, as the Indian diet is rich in herbs and spices, the incidence of Alzheimer's disease in India is considerably low (9,10). However, the precise molecular mechanisms of the therapeutic effects of medicinal herbs and spices are largely undefined, and limited data and a small body of convincing evidence exist at the molecular level (11).…”

Section: Introductionmentioning

confidence: 99%

Turmeric and curcumin suppress presenilin 1 protein expression in Jurkat cells

Yoshida¹,

Okumura²,

Nishimura³

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. In the present study, we aimed to determine the effects of herbs or spices on the expression of presenilin 1, a molecule involved in γ-secretase activity and the generation of amyloid-β peptide in Alzheimer's disease. Western blot analysis revealed that presenilin 1 protein expression was down-regulated by stimulation with turmeric or cinnamon extracts in vitro, while the effects on presenilin 1 gene expression examined by reverse transcriptase-polymerase chain reaction were unaltered. Our results showed that curcumin, a component of turmeric, induced the down-regulation of presenilin 1 protein in Jurkat and K562 cell lines. IntroductionAlzheimer's disease is a neurodegenerative disease caused by amyloid-β accumulation in brain cells combined with oxidative stress and inflammation (1,2). Neurotoxic amyloid-β is an approximately 4-kDa peptide generated via cleavage of the amyloid-β precursor protein (APP) by the γ-secretase proteolytic complex (3). Presenilin is the catalytic member of the γ-secretase complex, and mutations in presenilin are the major cause of early-onset familial Alzheimer's disease. Presenilin is involved in several biological functions, but is well known for its role in the generation of the amyloid-β peptide in Alzheimer's disease and is therefore thought to be an important drug target for this disorder. Thus, an increased understanding of Presenilin may help to improve the development of drugs for Alzheimer's disease and for other neurological diseases (4).Certain herbs have been demonstrated to possess a multitude of beneficial activities, and herbal medications are currently being used for widespread clinical use in disease therapy, as herbs exhibit relatively mild bioavailability and low toxicity (5). As for Alzheimer's disease, polyphenols extracted from grape seeds have been found to inhibit amyloid-β aggregation, reduce amyloid-β production and protect against amyloid-β neurotoxicity in vitro (6,7). In addition, cryptotanshinone (CTS), an active component of the medicinal herb Salvia miltiorrhiza, has been shown to improve learning and memory in several pharmacological models of Alzheimer's disease (8). Further research demonstrated that CTS improved the cognitive ability and promoted APP metabolism involving the non-amyloidogenic product pathway in rat cortical neuronal cells. Moreover, as the Indian diet is rich in herbs and spices, the incidence of Alzheimer's disease in India is considerably low (9,10). However, the precise molecular mechanisms of the therapeutic effects of medicinal herbs and spices are largely undefined, and limited data and a small body of convincing evidence exist at the molecular level (11). Therefore, basic research and development aimed at elucidating the mechanism of action underlying herbal effects should have high priority. We hypothesized that various herbs or spices may affect the γ-secretase proteolytic function. Therefore, we investigated the in vitro effect of several herbs on the expression of presenilin 1 in cultured human cells. Material...

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“…As the Indian diet is rich in certain spices, the prevalence of AD patients in India is considerably low (3). However, the precise molecular mechanism for the effect of these spices is largely undefined, and limited data and evidence have been provided at the molecular level (4).…”

Section: Introductionmentioning

confidence: 99%

Genistein downregulates presenilin 1 and ubiquilin 1 expression

et al. 2011

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Abstract. The aim of this study was to determine the effects of several food ingredients and chemical inhibitors on the expression of presenilin, a molecule involved in γ-secretase activity and the generation of amyloid-β peptide in Alzheimer's disease. Western blotting revealed the downregulation of presenilin 1 protein expression by stimulation with genistein in vitro, while the effects on presenilin 1 gene expression examined by reverse transcriptase-polymerase chain reaction (RT-PCR) were unaltered in Daudi cells. Genistein likely downregulates presenilin via the inhibition of ubiquilin 1 expression in lymphoid cells. Our findings provide new insights that may help to establish preventive strategies against Alzheimer's disease.

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Apolipoprotein E Polymorphism and Alzheimer Disease

Abstract: This first report of APOEE4 and AD from the Indian subcontinent shows very low prevalence of AD in Ballabgarh, India, but association of APOEE4 with AD at similar strength in Indian and US samples. Arch Neurol. 2000.

Cited by 296 publications

References 36 publications

Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

Turmeric and curcumin suppress presenilin 1 protein expression in Jurkat cells

Genistein downregulates presenilin 1 and ubiquilin 1 expression

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Apolipoprotein E Polymorphism and Alzheimer Disease

Abstract: This first report of APOE*E4 and AD from the Indian subcontinent shows very low prevalence of AD in Ballabgarh, India, but association of APOE*E4 with AD at similar strength in Indian and US samples. Arch Neurol. 2000.

Cited by 296 publications

References 36 publications

Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

Turmeric and curcumin suppress presenilin 1 protein expression in Jurkat cells

Genistein downregulates presenilin 1 and ubiquilin 1 expression

Contact Info

Product

Resources

About

Abstract: This first report of APOEE4 and AD from the Indian subcontinent shows very low prevalence of AD in Ballabgarh, India, but association of APOEE4 with AD at similar strength in Indian and US samples. Arch Neurol. 2000.