<?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>2221-2450</journal-id>
<journal-title><![CDATA[Revista CENIC Ciencias Biológicas]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. CENIC Cienc. Biol]]></abbrev-journal-title>
<issn>2221-2450</issn>
<publisher>
<publisher-name><![CDATA[Centro Nacional de Investigaciones Científicas]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2221-24502023000100044</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[INHIBIDORES DE LA ACTIVIDAD COLINESTERASA COMO TERAPIA SINTOMÁTICA PARA LA ENFERMEDAD DE ALZHEIMER]]></article-title>
<article-title xml:lang="en"><![CDATA[CHOLINESTERASE ACTIVITY INHIBITORS AS SYMPTOMATIC THERAPY FOR ALZHEIMER&#8217;S DISEASE]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Torres McCook]]></surname>
<given-names><![CDATA[Angel Ramón]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rodríguez Tanty]]></surname>
<given-names><![CDATA[Chryslaine]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[García Pupo]]></surname>
<given-names><![CDATA[Laura]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Centro de Neurociencias de Cuba  ]]></institution>
<addr-line><![CDATA[ La Habana]]></addr-line>
<country>Cuba</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>00</month>
<year>2023</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>00</month>
<year>2023</year>
</pub-date>
<volume>54</volume>
<fpage>44</fpage>
<lpage>68</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_arttext&amp;pid=S2221-24502023000100044&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_abstract&amp;pid=S2221-24502023000100044&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_pdf&amp;pid=S2221-24502023000100044&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN La enfermedad de Alzheimer es una de las principales causas de demencia en la actualidad. Este trastorno neurodegenerativo produce la disminución progresiva de la capacidad cognitiva y la memoria. Entre los procesos bioquímicos que caracterizan esta enfermedad se incluyen la formación de placas &#946;-amiloides, el desarrollo de nudos neurofibrilares, y la pérdida de neuronas colinérgicas en la corteza cerebral. De hecho, la mayoría de los medicamentos disponibles para enfrentar esta enfermedad están dirigidos a las afectaciones que sufren los individuos enfermos en la sinapsis colinérgica del Sistema Nervioso Central. Es por esta razón que el desarrollo de fármacos dirigidos a dianas terapéuticas que permitan incrementar la disponibilidad de acetilcolina en la sinapsis colinérgica es un campo de investigación de gran interés. Sin embargo, el éxito en el uso clínico de estos compuestos resulta limitado por los efectos secundarios que producen y por el carácter multifactorial de esta enfermedad. La presente revisión tiene como objetivo brindar una panorámica sobre la disfunción colinérgica observada en los pacientes de la enfermedad de Alzheimer y que sustenta la hipótesis colinérgica en su fisiopatología. Además, se profundiza en los inhibidores de la actividad colinesterasa de uso clínico e innovadores, como alternativa de terapia sintomática para la enfermedad de Alzheimer.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT Alzheimer's disease is one of the leading causes of dementia today. This neurodegenerative disorder results in the progressive decline of cognitive ability and memory. The biochemical processes that characterize this disease include the formation of &#946;-amyloid plaques, the development of neurofibrillary tangles, and the loss of cholinergic neurons in the cerebral cortex. In fact, most of the drugs available to deal with this disease are directed at the affectations suffered by diseased individuals in the cholinergic synapse of the Central Nervous System. It is for this reason that the development of drugs directed to therapeutic targets that allow increasing the availability of acetylcholine in the cholinergic synapse is a field of research of great interest. However, success in the clinical use of these compounds is limited by the side effects they produce and by the multifactorial nature of this disease. The present review aims to provide an overview of the cholinergic dysfunction observed in Alzheimer's disease patients that supports the cholinergic hypothesis in its pathophysiology. In addition, cholinesterase activity inhibitors of clinical and innovative use are discussed as an alternative symptomatic therapy for Alzheimer's disease.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[inhibición]]></kwd>
<kwd lng="es"><![CDATA[acetilcolinesterasa]]></kwd>
<kwd lng="es"><![CDATA[Hipótesis Colinérgica]]></kwd>
<kwd lng="en"><![CDATA[inhibition]]></kwd>
<kwd lng="en"><![CDATA[acetylcholinesterase]]></kwd>
<kwd lng="en"><![CDATA[Cholinergic Hypothesis]]></kwd>
</kwd-group>
</article-meta>
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