<?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>1657-9534</journal-id>
<journal-title><![CDATA[Colombia Médica]]></journal-title>
<abbrev-journal-title><![CDATA[Colomb. Med.]]></abbrev-journal-title>
<issn>1657-9534</issn>
<publisher>
<publisher-name><![CDATA[Universidad del Valle]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1657-95342016000400203</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Amyloid-beta immunotherapy: the hope for Alzheimer disease?]]></article-title>
<article-title xml:lang="es"><![CDATA[Inmunoterapia beta-amiloide: ¿la esperanza para la enfermedad de Alzheimer?]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Barrera-Ocampo]]></surname>
<given-names><![CDATA[Alvaro]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Lopera]]></surname>
<given-names><![CDATA[Francisco]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Icesi Facultad de Ciencias Naturales Departamento de Ciencias Farmacéuticas]]></institution>
<addr-line><![CDATA[Cali ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad de Antioquia Escuela de Medicina Grupo de Neurociencias de Antioquia]]></institution>
<addr-line><![CDATA[Medellin ]]></addr-line>
<country>Colombia</country>
</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>47</volume>
<numero>4</numero>
<fpage>203</fpage>
<lpage>212</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S1657-95342016000400203&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S1657-95342016000400203&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S1657-95342016000400203&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Alzheimer disease (AD) is the most prevalent form of dementia of adult-onset, characterized by progressive impairment in cognition and memory. There is no cure for the disease and the current treatments are only symptomatic. Drug discovery is an expensive and time-consuming process; in the last decade no new drugs have been found for AD despite the efforts of the scientific community and pharmaceutical companies. The A&#946; immunotherapy is one of the most promising approaches to modify the course of AD. This therapeutic strategy uses synthetic peptides or monoclonal antibodies (mAb) to decrease the A&#946; load in the brain and slow the progression of the disease. Therefore, this article will discuss the main aspects of AD neuropathogenesis, the classical pharmacologic treatment, as well as the active and passive immunization describing drug prototypes evaluated in different clinical trials.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La enfermedad de Alzheimer (EA) es la forma más frecuente de demencia de inicio en el adulto, caracterizada por un deterioro progresivo en la cognición y la memoria. No hay cura para la enfermedad y los tratamientos actuales son sólo sintomáticos. El descubrimiento de fármacos es un proceso costoso y que consume mucho tiempo; en la última década no se han encontrado nuevos fármacos para la EA a pesar de los esfuerzos de la comunidad científica y las compañías farmacéuticas. La inmunoterapia contra A&#946; es uno de los enfoques más prometedores para modificar el curso de la EA. Esta estrategia terapéutica utiliza péptidos sintéticos o anticuerpos monoclonales (mAb) para disminuir la carga de A&#946; en el cerebro y retardar la progresión de la enfermedad. Por lo tanto, este artículo discutirá los principales aspectos de la neuropatogénesis de la EA, el tratamiento farmacológico clásico, así como la inmunización activa y pasiva describiendo los prototipos de fármacos evaluados en diferentes ensayos clínicos.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Amyloid beta-Peptides]]></kwd>
<kwd lng="en"><![CDATA[antibodies]]></kwd>
<kwd lng="en"><![CDATA[cognitive dysfunction]]></kwd>
<kwd lng="en"><![CDATA[Alzheimer disease]]></kwd>
<kwd lng="en"><![CDATA[adult]]></kwd>
<kwd lng="en"><![CDATA[Immunotherapy]]></kwd>
<kwd lng="en"><![CDATA[Vaccination]]></kwd>
<kwd lng="en"><![CDATA[Immunization]]></kwd>
<kwd lng="es"><![CDATA[Péptidos beta-amiloide]]></kwd>
<kwd lng="es"><![CDATA[anticuerpos]]></kwd>
<kwd lng="es"><![CDATA[disfunción cognitiva]]></kwd>
<kwd lng="es"><![CDATA[Enfermedad de Alzheimer]]></kwd>
</kwd-group>
</article-meta>
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