Biomedical subjects

Lluís Tàrraga

Publications and source records attributed to Lluís Tàrraga.

4 recordsLinked to original sources

PubMed2005

Learning potential: a new method for assessing cognitive impairment.

BACKGROUND: In recent years, it has been claimed that learning potential (also called cognitive plasticity or rehabilitation potential) may be a good predictor of the course of cognitive impairment and the process of dementia. The basic objective of this research program is to test the extent to which the "Battery of Learning Potential for Assessing Dementia" (BEPAD) discriminates healthy people from those diagnosed with Mild Cognitive Impairment (MCI) and with Alzheimer's Disease (AD). METHODS: Two hundred people: 100 healthy elders (51 women, 49 men, mean age: 73.13), 50 diagnosed with MCI (30 women, 20 men, mean age: 74.89), and 50 diagnosed with mild AD (36 women, 14 men, mean age: 75.07). Learning potential was assessed through dynamic assessment (or testing-the-limits), using experimental test-training-post-test, a form of evaluation closely related to functional or stress testing in medicine. In several previous studies the BEPAD was developed, with four tasks: visuo-spatial, verbal recall (including delayed verbal recall), executive control and verbal fluency. For all of these tasks, training procedures were developed, converting them into learning potential tests. RESULTS AND CONCLUSIONS: All "dynamic" or learning scores (post-test) discriminate better healthy, MCI and AD subjects than all static or pre-test scores. A total of 89% of cases are correctly classified by the BEPAD: 95.7% of the healthy subjects, 90.6% of AD patients, and 71.1% of the MCI individuals were correctly classified.

Aged↗

PubMed2003

Association study between Alzheimer's disease and genes involved in Abeta biosynthesis, aggregation and degradation: suggestive results with BACE1.

BACKGROUND: Amyloid beta-peptide (Abeta) biosynthesis, aggregation and degradation constitute three important steps to consider in the study of pathological mechanisms involved in Alzheimer's disease (AD). Several proteins have been suggested as involved in each of these processes: proteolytic cleavage of the amyloid precursor protein by the beta-site APP cleaving enzyme (BACE), increased amyloid fibril formation by the activity of the acetylcholinesterase (ACHE gene), and degradation of Abeta aggregates by the plasmin system have been exhaustively documented. METHODS: A case-control design was used to evaluate the possible association between candidate genes involved in these three processes and AD. We analysed three polymorphisms located at the BACE1 gene, one polymorphism at the ACHE gene, and two variants located at the tissue plasminogen activator and plasminogen activator inhibitor-1 (genes TPA and PAI- 1, respectively), both part of the plasmin system. RESULTS: We found an association between BACE1 exon 5 GG genotype and AD (age-and gender-adjusted odds ratio = 2.14, P =0.014). Although a similar association was reported previously by Nowotny and collaborators only in subjects carrying the epsilon4-allele of the apolipoprotein E gene (APOE), we did not detect this effect. However,when we combined our results with those previously reported, a clear increase of the risk to develop AD appeared in subjects carrying both the BACE1 exon 5 GG genotype and the APOE epsilon4-allele (crude OR = 2.2, P = 0.004). CONCLUSION: These data suggest a possible genetic relation between BACE1 and AD.

3' Untranslated Regions↗

PubMed2003

Joint analysis of candidate genes related to Alzheimer's disease in a Spanish population.

BACKGROUND: Besides the repeated association between the epsilon 4 allele of the apolipoprotein E and Alzheimer's disease, several candidate genes have been analysed with inconsistent results. Most of these studies have examined only one or two polymorphisms in a defined population, which provides a lack of a general view of the Alzheimer's disease genetic component. OBJECTIVE: To overcome this limitation, nine polymorphisms in seven different candidate genes (A2M, ACT, APOE, APP, BH, HSP70-2, and IL1-A) were genotyped. METHODS: The sample comprised 112 Alzheimer's disease patients and 89 controls from Spain. Since haplotype reconstruction may add power to association studies, we also tested for linkage disequilibrium within the A2M and APOE genes. RESULTS: Except for the APOE gene, allele and genotype frequencies were not different between cases and controls, even when stratifying for the APOE genotype. CONCLUSION: The present results suggest that future association studies should be performed using a battery of polymorphisms in different and new candidate genes, taking into account the linkage disequilibrium in the region.

Alzheimer Disease↗

PubMed2003

HSP70-2 (HSPA1B) is associated with noncognitive symptoms in late-onset Alzheimer's disease.

Neuropsychiatric manifestations are common in Alzheimer's disease (AD) and their phenotypic expression might be related to physiopathological and genetic causes. Multiple studies have implicated oxidative stress to the pathogenesis and possible etiology of AD. One of the mechanisms to protect cells from oxidative stress is the expression of heat-shock proteins (HSP). HSPA1B (alternatively known as HSP70-2) has been related to AD pathophysiology. In the present analysis, 77 AD patients were classified according to their cognitive status with the Neuropsychiatric Inventory and were genotyped for an insertion/deletion (A1/A2) polymorphism. The A2 allele conferred a significant increase of psychiatric morbidity in an allele-dose manner (P < .05). This pattern can be attributed to all AD stages and the severity of the behavioral disturbances was higher for those patients carrying one or two A2 alleles. These results indicate a possible association between the A2 allele and an overexpression of noncognitive symptoms in AD.

Age Factors↗