<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1409-0015</journal-id>
<journal-title><![CDATA[Medicina Legal de Costa Rica]]></journal-title>
<abbrev-journal-title><![CDATA[Med. leg. Costa Rica]]></abbrev-journal-title>
<issn>1409-0015</issn>
<publisher>
<publisher-name><![CDATA[Asociación Costarricense de Medicina Forense]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1409-00152016000200104</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Biología molecular de la enfermedad de Alzheimer]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Carvajal Carvajal]]></surname>
<given-names><![CDATA[Carlos]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Hospital de Guápiles Laboratorio Clínico ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2016</year>
</pub-date>
<volume>33</volume>
<numero>2</numero>
<fpage>104</fpage>
<lpage>122</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_arttext&amp;pid=S1409-00152016000200104&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_abstract&amp;pid=S1409-00152016000200104&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_pdf&amp;pid=S1409-00152016000200104&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen: La enfermedad de Alzheimer (EA) es una enfermedad neurodegenerativa asociada con una disminución cognitiva y es la forma más común de demencia en los ancianos. Un gran número de factores se asocian con un riesgo aumentado de EA, no obstante, la edad representa, por mucho, el riesgo individual más grande en la etiología de la EA. La variante genética más fuerte para la EA típica de inicio tardío es la apolipoproteína E (APOE). Mutaciones raras en tres genes han sido implicadas en la enfermedad familiar de inicio temprano: APP, PSEN1 y PSEN2. Las placas amiloides extracelulares y los ovillos neurofibrilares intraneurales (NFT) son las dos lesiones características de esta enfermedad fatal. La proteína tau está involucrada en el ensamblaje y estabilización de los microtúbulos. La fosforilación anormal de tau, una característica prominente del cerebro con EA, decrece su habilidad de unión a los microtúbulos, pudiendo desestabilizar los microtúbulos y causar daño celular. Un grupo heterogéneo de péptidos A&#946; monoméricos de entre 37 a 43 aminoácidos se genera a partir de la proteína precursora amiloide transmembrana (APP) por el corte mediado por las secretasas &#946; y &#1509;. El monómero tiene una alta tendencia a autoagregarse formando agregados grandes y fibrillas. In vivo existe una sopa de oligómeros de A&#946; consistiendo de una gran variedad de formas intercambiables rápidamente, que difieren en tamaño, conformación, desorden intrínseco y toxicidad. Evidencia creciente sugiere que las formas más dañinas de los péptidos del amiloide &#946; son los oligómeros solubles y que los depósitos amorfos e insolubles o fibrilares representan una forma inactivada menos peligrosa del péptido. Varios mecanismos han sido propuestos para explicar las anormalidades en la EA, incluyendo la toxicidad por A&#946;, deficiencias del transporte axónico y el estrés oxidativo.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract: Alzheimer disease (AD is a progressive neurodegenerative disease associated with cognitive decline and is the most common form of dementia in the enderly. A large number of factors has been associated with increased risk of AD, however, age represents, by far, the single greatest risk factor in the etiology of AD. The strongest common genetic variant for typical late-onset AD is apoliprotein E (APOE). Rare mutations in three genes have been implicated in familial early-onset disease: APP, PSEN1, and PSEN2. Extracellular amyloid plaques and intraneuronal neurofibrillary tangles (NFT) are two major hallmark lesions of this fatal pathology. Tau protein is involved in microtubule assembly and stabilization. Abnormal phosphorylation of tau, a prominent feature of AD brain, decreases its microtubule binding ability, which may destabilize microtubules and results in cellular damage. A heterogeneous pool of monomeric A&#946; peptide varying in length from 37 to 43 amino acids is generated from the transmembrane amyloid precursor protein (APP) by &#946;- and &#1509;-secretase-mediated cleavage. The A&#946; monomer has a high tendency to self-assemble into large aggregates and fibrils. A diverse &#8220;A&#946; oligomeric soup&#8221; exists, consisting of a large variety of rapidly exchangeable polymorphs that differ in size, conformation, intrinsic disorder, and toxicity. Growing evidence suggests that the most detrimental forms of amyloid &#946; peptides are the soluble oligomers and that the insoluble amorphous or fibrillar deposits represent a less harmful inactivated form of the peptide. Several mechanisms have been proposed to account for abnormalities in AD, including A&#946; toxicity, axonal transport deficiencies, and oxidative stress.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Enfermedad de Alzheimer]]></kwd>
<kwd lng="es"><![CDATA[placas amiloides]]></kwd>
<kwd lng="es"><![CDATA[amiloide beta]]></kwd>
<kwd lng="es"><![CDATA[proteína tau]]></kwd>
<kwd lng="es"><![CDATA[desórdenes neurodegenerativos]]></kwd>
<kwd lng="es"><![CDATA[estrés oxidativo]]></kwd>
<kwd lng="en"><![CDATA[Alzheimer disease]]></kwd>
<kwd lng="en"><![CDATA[amyloid plaques]]></kwd>
<kwd lng="en"><![CDATA[amyloid beta]]></kwd>
<kwd lng="en"><![CDATA[tau protein]]></kwd>
<kwd lng="en"><![CDATA[neurodegenerative disorders]]></kwd>
<kwd lng="en"><![CDATA[oxidative stress]]></kwd>
</kwd-group>
</article-meta>
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