The role of lysosomes and autophagosomes in frontotemporal lobar degeneration.

INTRODUCTION: Cell biological and genetic evidence implicate failures in degrading aggregating proteins, such as tau and TDP-43, through the autophagy or lysosomal pathways in the pathogenesis of frontotemporal lobar degeneration (FTLD). METHODS: We investigated changes in the degradative pathways in 60 patients with different pathological or genetic forms of FTLD employing immunohistochemistry for marker proteins such as lysosomal-associated membrane proteins 1 (LAMP-1) and 2 (LAMP-2), cathepsin D (CTSD) and microtubule-associated protein 1 light chain 3 alpha (LC3A). Immunostained sections were qualitatively and semi-quantitatively assessed for the appearance, distribution and intensity of staining in neurones of the dentate gyrus (DG) and CA4 region of the hippocampus, and the temporal cortex (Tcx). RESULTS: Lower levels of neuronal LAMP-1 immunostaining were present in the DG and Tcx in FTLD-tau compared to FTLD-TDP. There was less LAMP-1 immunostaining in FTLD-tau with MAPT mutations, and FTLD-tau with Pick bodies, compared to FTLD-TDP types A and B, and less LAMP-1 immunostaining in FTLD-TDP type C than in FTLD-TDP types A and B. There was greater LAMP-1 immunostaining in GRN mutation which may reflect the underlying type A histology rather than mutation. There were no differences in neuronal LAMP-2, CTSD, EEA-1 or LC3A immunostaining between any of the five FTLD histological or four genetic groups, nor between FTLD-TDP and FTLD-tau. CONCLUSIONS: The underlying pathological mechanism in FTLD-tau may lie with a relative deficiency of lysosomes, or defective vesicular transport, whereas the failure to clear TDP-43 aggregates may lie with lysosomal dysfunction rather than a lack of available lysosomes or degradative enzymes.

Neurodegeneration in frontotemporal lobar degeneration and motor neurone disease associated with expansions in C9orf72 is linked to TDP-43 pathology and not associated with aggregated forms of dipeptide repeat proteins.

AIMS: A hexanucleotide expansion in C9orf72 is the major genetic cause of inherited behavioural variant Frontotemporal dementia (bvFTD) and motor neurone disease (MND), although the pathological mechanism(s) underlying disease remains uncertain. METHODS: Using antibodies to poly-GA, poly-GP, poly-GR, poly-AP and poly-PR proteins, we examined sections of cerebral cortex, hippocampus, thalamus, cerebellum and spinal cord, from 20 patients with bvFTD and/or MND bearing an expansion in C9orf72 for aggregated deposits of dipeptide repeat proteins (DPR). RESULTS: Antibodies to poly-GA, poly-GP and poly-GR detected numerous rounded cytoplasmic inclusions (NCI) within granule cells of hippocampal dentate gyrus and those of the cerebellum, as well as 'star-burst' shaped NCI in pyramidal neurones of CA3/4 region of hippocampus. NCI were uncommon in Purkinje cells, and only very rarely seen in anterior horn cells. Poly-PA antibody detected occasional NCI within CA3/4 neurones alone, whereas poly-PR antibody did not identify any NCI but immunostained the nucleus of anterior horn cells, CA3/4 neurones and Purkinje cells, in patients with or without expansion in C9orf72, as well as in normal controls. Poly-GA antibody generally detected more DPR than poly-GP, which in turn was greater than poly-GR. All patients with bvFTD + MND or MND showed plentiful p62/TDP-43 positive inclusions in remaining anterior horn cells. CONCLUSION: Degeneration and loss of anterior horn cells associated with expansions in C9orf72 occurs in the absence of DPR, and implies that changes involving loss of nuclear staining for and a cytoplasmic aggregation of TDP-43 are more likely to be the cause of this.

Patterns of cerebral amyloid angiopathy define histopathological phenotypes in Alzheimer's disease.

AIMS: Pathological heterogeneity of Aß deposition in senile plaques (SP) and cerebral amyloid angiopathy (CAA) in Alzheimer's disease (AD) has been long noted. The aim of this study was to classify cases of AD according to their pattern of Aß deposition, and to seek factors which might predict, or predispose towards, this heterogeneity. METHODS: The form, distribution and severity of Aß deposition (as SP and/or CAA) was assessed semiquantitatively in immunostained sections of frontal, temporal and occipital cortex from 134 pathologically confirmed cases of AD. RESULTS: Four patterns of Aß deposition were defined. Type 1 describes cases predominantly with SP, with or without CAA within leptomeningeal vessels alone. Type 2 describes cases where, along with many SP, CAA is present in both leptomeningeal and deeper penetrating arteries. Type 3 describes cases where capillary CAA is present along with SP and arterial CAA. Type 4 describes a predominantly vascular phenotype, where Aß deposition is much more prevalent in and around blood vessels, than as SP. As would be anticipated from the group definitions, there were significant differences in the distribution and degree of CAA across the phenotype groups, although Aß deposition as SP did not vary. There were no significant differences between phenotype groups with regard to age of onset, age at death, disease duration and brain weight, or disease presentation. Women were over-represented in the type 1 phenotype and men in type 2. Genetically, type 3 (capillary subtype) cases were strongly associated with possession of the APOE ε4 allele. CONCLUSIONS: This study offers an alternative method of pathologically classifying cases of AD. Further studies may derive additional genetic, environmental or clinical factors which associate with, or may be responsible for, these varying pathological presentations of AD.

Nuclear carrier and RNA-binding proteins in frontotemporal lobar degeneration associated with fused in sarcoma (FUS) pathological changes.

AIMS: We aimed to investigate the role of the nuclear carrier and binding proteins, transportin 1 (TRN1) and transportin 2 (TRN2), TATA-binding protein-associated factor 15 (TAF15) and Ewing's sarcoma protein (EWS) in inclusion body formation in cases of frontotemporal lobar degeneration (FTLD) associated with fused in sarcoma protein (FTLD-FUS). METHODS: Eight cases of FTLD-FUS (five cases of atypical FTLD-U, two of neuronal intermediate filament inclusion body disease and one of basophilic inclusion body disease) were immunostained for FUS, TRN1, TRN2, TAF15 and EWS. Ten cases of FTLD associated with TDP-43 inclusions served as reference cases. RESULTS: The inclusion bodies in FTLD-FUS contained TRN1 and TAF15 and, to a lesser extent, EWS, but not TRN2. The patterns of immunostaining for TRN1 and TAF15 were very similar to that of FUS. None of these proteins was associated with tau or TDP-43 aggregations in FTLD. CONCLUSIONS: Data suggest that FUS, TRN1 and TAF15 may participate in a functional pathway in an interdependent way, and imply that the function of TDP-43 may not necessarily be in parallel with, or complementary to, that of FUS, despite each protein sharing many similar structural elements.

Post mortem cerebrospinal fluid α-synuclein levels are raised in multiple system atrophy and distinguish this from the other α-synucleinopathies, Parkinson's disease and Dementia with Lewy bodies.

Differentiating clinically between Parkinson's disease (PD) and the atypical parkinsonian syndromes of Progressive supranuclear palsy (PSP), corticobasal syndrome (CBS) and multiple system atrophy (MSA) is challenging but crucial for patient management and recruitment into clinical trials. Because PD (and the related disorder Dementia with Lewy bodies (DLB)) and MSA are characterised by the deposition of aggregated forms of α-synuclein protein (α-syn) in the brain, whereas CBS and PSP are tauopathies, we have developed immunoassays to detect levels of total and oligomeric forms of α-syn, and phosphorylated and phosphorylated oligomeric forms of α-syn, within body fluids, in an attempt to find a biomarker that will differentiate between these disorders. Levels of these 4 different forms of α-syn were measured in post mortem samples of ventricular cerebrospinal fluid (CSF) obtained from 76 patients with PD, DLB, PSP or MSA, and in 20 healthy controls. Mean CSF levels of total and oligomeric α-syn, and phosphorylated α-syn, did not vary significantly between the diagnostic groups, whereas mean CSF levels of phosphorylated oligomeric α-syn did differ significantly (p<0.001) amongst the different diagnostic groups. Although all 4 measures of α-syn were higher in patients with MSA compared to all other diagnostic groups, these were only significantly raised (p<0.001) in MSA compared to all other diagnostic groups, for phosphorylated oligomeric forms of α-syn. This suggests that this particular assay may have utility in differentiating MSA from control subject and patients with other α-synucleinopathies. However, it does not appear to be of help in distinguishing patients with PD and DLB from those with PSP or from control subjects. Western blots show that the principal form of α-syn within CSF is phosphorylated, and the finding that the phosphorylated oligomeric α-syn immunoassay appears to be the most informative of the 4 assays would be consistent with this observation.

Suicide ideation in Jamaican youth: sociodemographic prevalence, protective and risk factors.

OBJECTIVE: To determine the prevalence of suicidal ideation and examine the association between suicidal ideation and sociodemographic characteristics, protective and risk factors among Jamaican youth. METHOD: In this cross-sectional study, an interviewer administered school-based survey was conducted among 2997 students 10-15 years old in Jamaica. Although there were a number of questions on suicide, this paper focusses on one question "During the past year did you ever seriously consider attempting suicide?" as the measure of suicidal ideation. RESULTS: The prevalence rate of suicidal ideation was 9.7%. Logistic regression analysis revealed that significant correlates of suicidal ideation were being female (odds ratio = 1.49), being depressed (odds ratio = 5.78), living in a rural area (odds ratio = 0.62), likes oneself (odds ratio = 0.58), indulging in aggressive behaviour (odds ratio = 1.43), has considered harming others (odds ratio = 3.11), protective factors in the home (odds ratio = 0.62), involvement in risky behaviour (odds ratio = 1.56) and being teased/bullied (odds ratio = 1.69). CONCLUSION: These findings have implication for prevention and treatment of suicidal behaviour in children and adolescents.

Depressive symptoms in adolescents in Jamaica.

BACKGROUND: Depression in adolescents is often overlooked and misdiagnosed; however it is an important mental health problem which is associated with major functional impairments across daily domains of living, and considerable morbidity. The aim of this research is to examine the prevalence of self-reported depressive symptoms among Jamaican adolescents, and the associated sociodemographic factors. SUBJECTS AND METHOD: This cross-sectional study included 3003 students between 10 and 15 years old in Jamaica. Survey methodology was used in the collection of the data. RESULTS: Of the sample of students, 47% were males. One hundred and thirty-four (4.5%) reported having depressive symptoms. The factors significantly associated with depressive symptoms were negative community attributes (B = 1.1; p = 0.001), protective factors within the home (B = 0.72; p = 0.000), gender (B = 1.92; p = 0.000), and learning problems (B = 3.1; p = 0.000). CONCLUSION: Results indicate rates of depressive symptomatology reported among adolescents in Jamaica are consistent with rates reported in the literature.

Influence and interactions of cathepsin D, HLA-DRB1 and APOE on cognitive abilities in an older non-demented population.

Cathepsin D (CTSD), human leukocyte antigen DRB1 (HLA-DRB1) and apolipoprotein E (APOE) have all been associated with cognitive ability in both demented and non-demented individuals. CTSD is a pleiotrophic protein whose functions include the processing of proteins prior to presentation by HLA. Several studies have also reported that a functional exon 2 polymorphism in the CTSD gene interacts with APOEepsilon4 resulting in an increased risk of developing Alzheimer's disease (AD). We have previously reported that the CTSD exon 2 polymorphism regulates fluid intelligence. In this study, we extend this finding to other cognitive domains and investigate interactions with APOE and HLA-DRB1. Using a cohort of 766 non-demented volunteers, we found that the CTSD exon 2 T allele was associated with a decrease in several cognitive domains that comprise processing speed [random letters (RLs) test, P = 0.012; alphabet-coding task (ACT), P = 0.001], spatial recall (SR) (P = 0.016) and an additional test of fluid intelligence (P = 0.010). We also observed that the HLA-DR1 was associated with enhanced cumulative recall ability (P = 0.006), and conversely HLA-DR5 was associated with diminished delayed verbal recall and SR abilities (P = 0.014 and P = 0.003, respectively). When analysed independently, APOEepsilon4 did not influence any cognitive domains. In contrast, CTSD T/APOEepsilon4-positive volunteers scored lower on tests of fluid intelligence (P = 0.015), processing speed (ACT, P = 0.001; RL, P = 0.013) and immediate recall (P = 0.029). Scores were lower for all these tests than when CTSD and APOE were analysed independently. This supports previous findings in AD that have also reported an epistatic interaction. In addition, we found that CTSD T/HLA-DR2-positive volunteers had reduced processing speed (ACT, P = 0.040; RL, P = 0.014) and had significantly lower cumulative and SR abilities (P = 0.003 and P = 0.001, respectively). Biological interaction between these two proteins has previously been shown where HLA-DR2 binds more readily to the myelin basic protein (MBP) compared with other DR antigens, preventing MBP cleavage by CTSD.

Age-associated changes in neuroaxonal transport in the hypothalamo-neurohypophysial system of the mouse.

In this study, we investigated age-associated changes in neuroaxonal transport of the hormone vasopressin (AVP) and its associated neurophysin (NPII), from the supraoptic nucleus (SON) of the hypothalamus to the neurohypophysis. C57BL/Icrfat male mice of 6 and 28 months of age were injected in the hypothalamus with L-[35S]cysteine. Animals were killed up to 2.25 h after injection and NPII and AVP from the SON and neurohypophysis were separated using HPLC, and the fractions counted for radioactivity. In the SON, radiolabelled NPII and AVP were first detected after 0.50 h in both young and old mice. There was no significant difference between the age-groups in the incorporation of radiolabel over the time course studied. Radiolabelled NPII in the neurohypophysis was significantly above background after 1.25 h in the young, and after 1.50 h in the old mice. The differences between the two age groups was significant (P = 0.05). Radiolabelled AVP followed a similar trend, but was not significantly above background until 1.50 h in the young and 1.75 h in the old. The differences between the two age groups was on the point of significance (P = 0.056). These results indicate a significant reduction of up to 25% in the rate of axonal transport of neurohypophyseal peptides with advancing age.

The ageing hypothalamo-neurohypophysial system. An analysis of the neurohypophysis in normal hydration, osmotic loading and rehydration.

Age-associated changes in the structure and function of the neurohypophysis may contribute to the decreased ability to conserve water in older animals. We investigated the neurohypophyses of 6 and 28-month-old male mice using radioimmunoassay and quantitative morphological techniques. The dry-weight and volume of the neurohypophysis increased significantly with age but the quantity of vasopressin in the gland remained constant. Oxytocin levels decreased with age. A quantitative morphological analysis was performed on the compartments of the neurohypophysis from male mice of 6 and 28 months of age which were either normally hydrated, osmotically loaded, or osmotically loaded and rehydrated. The absolute volumes of the axon endings, swellings, their constituent organelles and the axon terminals containing degenerating subcellular components were determined. The design of the analysis allowed us to examine both age-related changes and statistical interactions between the age of the animal and the behaviour of a variable during the osmotic loading/rehydration phase of the experiment. There was a significant age-related reduction in the volume of the neurohypophysis occupied by the endings and swellings. The diameters of the neurosecretory granules found in the endings were significantly smaller than those in the swellings in both age groups but the size difference was greater in the young animals. Dehydration and subsequent rehydration of old male mice leads to extensive re-modelling of the neurohypophysial compartments and subcellular organelles to the configuration found in the adult animal.

Renal vasopressin receptors in ageing C57BL/Icrfat mice.

The mechanism of water conservation is impaired in ageing mammals. An age-related defect in the release of vasopressin has been implicated but, more recently, attention has moved to the renal component of the water conservation mechanism. Previous studies using renal cells prepared from mice of different ages have shown that the threshold dose of vasopressin required to elicit a significant rise in cyclic AMP (cAMP) was greater in older animals. The dose-response curve was moved to the right in 35-month-old mice, i.e. the concentration of vasopressin required to give maximum cAMP output was increased. To investigate this further we examined the binding of vasopressin to renal medullary cells maintained in short-term culture, to determine whether the decreased response of cAMP levels to vasopressin is due to changes in hormone-receptor interaction. In 6-month-old male mice the dissociation constant (Kd) was 2.38 nmol/l and the maximum binding of the hormone (Bmax) was 47.6 fmol/10(6) cells, and at 30 months of age Kd was 2.37 nmol/l and Bmax was 47.0 fmol/10(6) cells. In female mice the changes were more complicated because the data for the 6-month-old mice could be split into two groups. It is concluded that there are no age-related differences in the numbers of receptors or their affinity for vasopressin, and that the decreased cAMP response is probably associated with post-receptor mechanisms in this species.

Effect of ageing on cyclic AMP output by renal medullary cells in response to arginine vasopressin in vitro in C57BL/Icrfat mice.

The effect of age on the cyclic AMP (cAMP) response to increases in the concentration of arginine vasopressin in the presence of isobutyl methylxanthine (100 mumol/l) was studied in an in-vitro renal cell suspension prepared from C57BL/Icrfat mice at 6, 12, 18, 24, 29 and 35 months of age. Comparison of the response of the preparation to vasopressin, calcitonin and parathyroid hormone suggested that it was enriched with renal medullary cells. Basal cAMP output was similar throughout but the threshold dose of vasopressin increased from 1 X 10(-11) mol/l (6, 12 and 18 months of age) to 1 X 10(-10) mol/l (24, 29 and 35 months of age). The dose-response curve in 35-month-old mice was shifted to the right with the concentration of vasopressin required to give half maximal cAMP increased from 9.4 +/- 0.37 X 10(-11) mol/l (6 months) to 3.5 +/- 1.6 X 10(-10) mol/l (35 months). Maximum cAMP output at 1 X 10(-9) mol/l was also reduced in the same animals (stimulated:basal ratio, 51.22 +/- 19.12 at 6 months; 11.50 +/- 6.02 at 35 months). The results suggest that the lack of renal response to vasopressin in terms of cAMP metabolism may play a role in the well-documented age-related decline in urine-concentrating ability in experimental animals and elderly people.

The effect of vitamin E deficiency on the induction of age pigment in various tissues of the mouse.

The effect of a dietary deficiency of vitamin E on the concentrations of lipofuscin in the hippocampus and the supraoptic nucleus (SON) of the hypothalamus, and in adrenal cortical cells was assessed in male mice. The animals were fed either a control diet or the vitamin E deficient diet after 2 months of age for a period of 6 months. There was no significant difference in the growth curves of the 2 groups of animals over the period studied. Fluorescence microscopy and transmission electron microscopy were used to assess the effect of the diet on lipofuscin in the different tissues. Quantitative morphological techniques were used to determine the relative volumes of lipofuscin in the neurons from the SON and in the adrenal cortical cells. There was no significant difference in the concentration of lipofuscin in the SON neurons after vitamin E deficiency but there was a significant increase in the adrenal cortical cells. There was a clear difference in the effect of the deficiency on mitotic and fixed post-mitotic cells over the period investigated but further studies would be necessary to determine whether or not there was a critical period in the life span where vitamin E deficiency may induce changes in all cell types.

Age-related postreceptor mechanisms: changes in adenylate cyclase but not phosphodiesterase in isolated mouse renal medullary collecting ducts.

Urine concentrating ability declines with increasing age, partly due to an impaired response of kidney medullary collecting ducts to the antidiuretic hormone, vasopressin. We investigated this change in isolated mouse medullary collecting ducts by measuring the activity of adenylate cyclase and phosphodiesterase, which catalyse the formation and hydrolysis of cAMP, respectively. Adenylate cyclase activity was measured in the presence of vasopressin (which stimulates adenylate cyclase via the receptor) or forskolin (which directly stimulates the catalytic subunit). We showed an age-related decrease in the catalytic subunit of adenylate cyclase, and no difference in the activity of phosphodiesterase, indicating that a reduction in the catalytic subunit of adenylate cyclase contributes towards the age-related decrease in cyclic AMP response of kidney to vasopressin.

The effect of aging on skeletal muscle capillarization in a murine model.

Capillarization of skeletal muscle has been reported to be both maintained and reduced with advancing age. This conflict may represent methodological differences between biopsy studies. We have examined capillarization throughout two muscles, soleus and extensor digitorum longus (EDL), from a well-established colony of aging mice, and related this to fiber number (C/F ratio) and type. Labeling of muscle capillaries was performed with the biotinylated Griffonia (Bandeiraea) simplicifolia lectin (GSL 1) using immunochemistry. The results showed a significant increase in the C/F ratio in the aged mice when compared with the younger (6-month mice soleus = 1.296, 95% CI 1.226-1.366 vs 28-month mice soleus = 1.530, 95% CI 1.488-1.572, p <.001; 6-month mice EDL = 0.881, 95% CI 0.751-1.011 vs 28-month mice EDL = 1.124, 95% CI 1.028-1.220, p = .017). These differences could not be accounted for by changes in fiber type but may reflect loss of fibers. Alternatively, there may be increased angiogenic drive or a failure of downregulation of angiogenesis.

Depressive symptoms in adolescents in Jamaica / Síntomas depresivos en adolescentes de Jamaica

BACKGROUND: Depression in adolescents is often overlooked and misdiagnosed; however, it is an important mental health problem which is associated with major functional impairments across daily domains of living, and considerable morbidity. The aim of this research is to examine the prevalence of self-reported depressive symptoms among Jamaican adolescents, and the associated sociodemographic factors. SUBJECTS AND METHOD: This cross-sectional study included 3003 students between 10 and 15 years old in Jamaica. Survey methodology was used in the collection of the data. RESULTS: Of the sample of students, 47% were males. One hundred and thirty-four (4.5%) reported having depressive symptoms. The factors significantly associated with depressive symptoms were negative community attributes (B = 1.1; p = 0.001), protective factors within the home (B = 0.72; p = 0.000), gender (B = 1.92; p = 0.000), and learning problems (B = 3.1; p = 0.000). CONCLUSION: Results indicate rates of depressive symptomatology reported among adolescents in Jamaica are consistent with rates reported in the literature.

ANTECEDENTES: La depresión en los adolescentes es a menudo pasada por alto y mal diagnosticada, a pesar de que constituye un problema de salud mental importante. El mismo se halla asociado con deterioros funcionales mayores en todos los dominios de la vida diaria, y conlleva una morbosidad considerable. El objetivo de esta investigación es examinar la prevalencia de síntomas depresivos autoreportados entre adolescentes jamaicanos, así como pasar revista a los factores sociodemográficos asociados. MÉTODO: Este estudio transversal incluyó 3003 estudiantes jamaicanos entre 10 y 15 años de edad. La metodología de encuestas fue usada en la recogida de datos. RESULTADOS: De la muestra de estudiantes, 47% eran varones. Ciento treinta y cuatro (4.5%) reportaron tener síntomas depresivos. Los factores significativamente asociados con los síntomas de depresión fueron atributos comunitarios negativos (B = 1.1; p = 0.001), factores de protección en el hogar (B = 0.72; p = 0.000), género (B = 1.92; p = 0.000), y problemas de aprendizaje (B = 3.1; p = 0.000). CONCLUSIÓN: Los resultados indican que las tasas de sintomatología depresiva reportadas entre los adolescentes en Jamaica concuerdan con las tasas reportadas en la literatura.

Suicide ideation in Jamaican youth: sociodemographic prevalence, protective and risk factors / Ideación suicida en la juventud jamaicana: prevalencia sociodemográfica, factores de riesgo y factores de protección

OBJECTIVE: To determine the prevalence of suicidal ideation and examine the association between suicidal ideation and sociodemographic characteristics, protective and risk factors among Jamaican youth. METHOD: In this cross-sectional study, an interviewer administered school-based survey was conducted among 2997 students 10-15 years old in Jamaica. Although there were a number of questions on suicide, this paper focusses on one question "During the past year, did you ever seriously consider attempting suicide?" as the measure of suicidal ideation. RESULTS: The prevalence rate of suicidal ideation was 9.7%. Logistic regression analysis revealed that significant correlates of suicidal ideation were being female (odds ratio = 1.49), being depressed (odds ratio = 5.78), living in a rural area (odds ratio = 0.62), likes oneself (odds ratio = 0.58), indulging in aggressive behaviour (odds ratio = 1.43), has considered harming others (odds ratio = 3.11), protective factors in the home (odds ratio = 0.62), involvement in risky behaviour (odds ratio = 1.56) and being teased/bullied (odds ratio = 1.69). CONCLUSION: These findings have implication for prevention and treatment of suicidal behaviour in children and adolescents.

OBJETIVO: Determinar la prevalencia de ideación suicida y examinar la asociación entre la ideación suicida y las características sociodemográficas, así como los factores de protección y riesgo entre la juventud jamaicana. MÉTODO: En este estudio transversal, un entrevistador administró una encuesta escolar entre 2997 estudiantes de 10-15 años de edad en Jamaica. Aunque había varias preguntas sobre el suicidio, el documento se centraba en la siguiente, con el objeto de medir la ideación suicida: "¿Consideraste alguna vez seriamente cometer suicidio el año pasado?" RESULTADOS: La tasa de prevalencia de ideación suicida fue 9.7%. El análisis de regresión logística reveló que los correlatos significativos de ideación suicida fueron: ser mujer (cociente de probabilidades OR = 1.49), estar deprimido (cociente de probabilidades OR = 5.78), vivir en un área rural (cociente de probabilidades OR = 0.62), gustarse a sí mismo (cociente de probabilidades OR = 0.58), permitirse un comportamiento agresivo (cociente de probabilidades OR = 1.43), considerar hacer daño a otros (cociente de probabilidades OR = 3.11), factores de protección en la casa (cociente de probabilidades OR = 0.62), involucrarse en conductas arriesgadas (cociente de probabilidades OR = 1.56) y ser víctima de burla o acoso abusivo (cociente de probabilidades OR = 1.69). CONCLUSIÓN: Estos hallazgos tienen implicaciones en cuanto a prevenir y tratar la conducta suicida en niños y adolescentes.