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Francesco Panza

Publications and source records attributed to Francesco Panza.

43 records · Page 3Linked to original sources
PubMed2004

Vascular genetic factors and human longevity.

Complex inter-relationships between age-associated illnesses, such as vascular disease and Alzheimer's disease (AD), suggest that biological and genetic pathways may be worthy of examination in centenarian populations to provide insights into human longevity. This is also borne out by the involvement of lipoprotein metabolism and a number of vascular genetic risk factors. Repeated findings of a higher frequency of the apolipoprotein E (APOE) epsilon4 allele in middle-aged subjects compared with centenarians were reported. Furthermore, we have also shown how in different populations there is a significant trend in reduction of serum APOE levels from APOE epsilon2- to epsilon4-carrier as well as significant differences in serum APOE levels respect to age in epsilon4-carriers but only after adjustment for HDL cholesterol. In contrast, findings of increased prevalence of the angiotensin I converting enzyme 1 (ACE1) D allele in French centenarians have not been replicated, suggesting the possibility that regional differences may occur in ACE1(*)D frequency within Europe in centenarians, as has been recently reported for APOE epsilon2 and epsilon4 alleles. A number of studies have examined the potential role in longevity of other genes involved in vascular risk, haemostasis, and blood pressure regulation [methyltetrahydrofolatereductase (MTHFR), apolipoprotein A1 (APOA-I), apolipoprotein C3 (APOC-III), apolipoprotein A4 (APOA-IV), paraoxonase 1 (PON1), plasminogen activator inhibitor type I (PAI-1)], with contrasting results. While further studies are needed to confirm the possible role of APOE concentration as putative longevity factor, this paper provides an overview of genetic vascular factors potentially involved in human longevity.

Aging↗
PubMed2003

Apolipoprotein E (APOE) polymorphism influences serum APOE levels in Alzheimer's disease patients and centenarians.

Vascular factors may play a role in the etiology of Alzheimer's disease (AD) and increased serum apolipoprotein E (APOE) levels in AD could be of interest, as APOE concentration is associated with vascular disease. Aims of this study were to evaluate the influence of APOE genotype on serum APOE levels, and, secondly, to study serum APOE concentrations in relation to age and AD. APOE genotypes, serum total cholesterol, LDL cholesterol, HDL cholesterol, total cholesterol/HDL cholesterol ratio, triglycerides, and serum APOE were performed on 52 healthy centenarians, 49 AD patients, 45 age-matched controls, and 72 young healthy adults. In all study population a significant trend in reduction of serum APOE levels from APOE epsilon2- to epsilon4 carriers was observed. The difference in serum APOE levels among age groups significantly decreased in epsilon4 carriers only, including HDL cholesterol; no significant differences between AD patients and age-matched controls were found. In these highly selected populations, APOE genotype distribution strongly influences serum APOE concentration, not suggesting, at present, a possible role as a biochemical marker for AD, but only as a putative longevity factor.

Adult↗
PubMed2003

Angiotensin I converting enzyme (ACE) gene polymorphism in centenarians: different allele frequencies between the North and South of Europe.

Variants of the angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 (ACE1) gene and the apolipoprotein E gene (APOE) have been suggested to be associated with human longevity. We tested the association between the ACE1 insertion (I allele)/deletion (D allele) polymorphism and longevity in a population from Southern Italy and examined the impact of geographical variation on ACE1 allele frequencies on reported associations from other European countries. ACE1 and APOE genotypes were obtained on 82 centenarians and 252 middle-aged, unrelated subjects or volunteers. No statistically significant differences were found in ACE1 genotype or allele frequencies between centenarians and controls in this Southern Italian population nor was there any observed interaction with APOE alleles that are also reputed to be linked to longevity. However, decreasing gradients in ACE1*I allele frequencies, both in centenarians and controls, with concomitant increases in ACE1*D allele frequencies (particularly the ACE1*D/*D genotype) were observed to be statistically significant from Northern to Southern regions of Europe. These findings did not support the previously reported association between ACE1 polymorphism and longevity. However, there were interesting and significant differences, as one moves from Northern to Southern Europe, with regard to the distribution of ACE1 alleles. Such genetic differences in conjunction with differing environmental factors may explain in part previous results suggesting a role of this polymorphism in longevity.

Adult↗
PubMed2002

Relation of lipoprotein(a) as coronary risk factor to type 2 diabetes mellitus and low-density lipoprotein cholesterol in patients > or =65 years of age (The Italian Longitudinal Study on Aging).

High levels of serum lipoprotein(a) [Lp(a)] have been associated with increased risk of coronary artery disease (CAD), but this association apparently is not confirmed in elderly people. We evaluated the interactions of Lp(a) with lipid and nonlipid CAD risk factors in a sample of subjects enrolled in the prevalence survey (1992 to 1993) of the Italian Longitudinal Study on Aging (ILSA). The entire population consisted of 5,632 elderly people, aged 65 to 84 years, randomly selected in 8 Italian municipalities. The present cross-sectional study included 400 free-living elderly subjects (74 +/- 6 years) from the randomized cohort of Casamassima (Bari, Southern Italy) (n = 704). The results showed that in the elderly population, high serum Lp(a) is a CAD risk factor dependent on type 2 diabetes mellitus and elevated low-density lipoprotein (LDL) cholesterol levels. In particular, the combined effect of high Lp(a) (> or =20 mg/dl) and high LDL cholesterol (> or =3.63 mmol/L [> or =140 mg/dl]), increases coronary risk by 2.75 (95% confidence interval 7.70 to 0.99); finally, the effect of Lp(a) > or =20 mg/dl and LDL cholesterol > or =3.63 mmol/L (> or =140 mg/dl), combined with type 2 diabetes mellitus, increases risk of CAD by 6.65 (95% confidence interval 35.40 to 1.25). In the elderly, elevated Lp(a) levels appear not to be an independent predictor of CAD, but this lipoprotein is a risk factor only in subjects with type 2 diabetes mellitus and elevated LDL cholesterol.

Aged↗
PubMed2002

Selective attention skills in differentiating between Alzheimer's disease and normal aging.

We determined the reliability and validity of a cancellation test of symbols (Symbol Cancellation Test [SCT]), designed to assess visual selective attention deficits in the elderly, on 34 Alzheimer's disease (AD) patients from Bari University Hospital Center, Bari, Italy, and 232 nondemented elderly subjects, aged 68 to 87 years, from the second prevalence survey (1995 through 1996) of the Italian Longitudinal Study on Aging (Casamassima, Bari, Italy). To assess convergent and discriminant validity, the Digit Cancellation Test (DCT), Mini-Mental State Examination (MMSE), and Babcock Story Recall Test (BSRT) were administered. Finally, discriminant accuracy of SCT between AD patients and nondemented elderly subjects was assessed. Inter-rater and test-retest reliability for P1 and P2 was excellent for both AD patients and the normal population, with a high degree of internal consistency. The SCT was significantly correlated with the DCT (0.67), MMSE (0.60), and BSRT (0.33). The classification accuracies of overall performance on the SCT for subjects with and without AD were 0.62 and 0.91, respectively. The SCT is a valid and reliable test to assess selective attention in elderly subjects, in whom dementing illness must be diagnosed and clinically distinct from age-related cognitive decline.

Age Factors↗
PubMed2002

[Genetics of late-onset Alzheimer's disease: vascular risk and beta-amyloid metabolism].

Progress in clinical and basic research of Alzheimer's disease (AD) suggested theoretical models of possible pathogenetic mechanisms, with a primary role of the genetic factors that have been implicated in AD. These can be divided into two main categories. First, the three genes in which mutations are known to result in early onset autosomal dominant familial AD (presenilins 1 and 2, and amyloid beta protein precursor [APP]): well characterized but that account for only a small proportion of AD cases. Secondly, late onset, sporadic AD is more common and evidence suggests that there is a genetic component to this type of disease. A number of genetic risk factors have been implicated that might increase the risk of developing sporadic disease: particularly, apolipoprotein E (apo E) polymorphism and many others suggested by linkage studies [alpha-macroglobulin, low density receptor protein (LRP1), bleomycin hydrolase], with a precise role in beta-amyloid metabolism and deposition. Many of these are controversial and studies have shown conflicting results, but apoE polymorphism seems to be only one of the possible genetic factors suggested to play a role in the multifactoral pathogenesis of AD. Regional and ethnic differences may affect the strength of association between apoE epsilon 4 allele and the disease, and we reported evidences of the decreasing frequency of epsilon 4 allele in AD patients and centenarians from Northern to Southern European regions. Finally, several genetic risk factors of vascular origin (angiotensin converting enzyme, methyltetrahydropholate-reductase, and NOS3 gene polymorphisms) have been implicated in the development of both vascular dementia and AD with conflicting results.

Age Factors↗