ENFERMEDAD DE ALZHEIMER

La reunión de Otoño del Grupo de Demencia de la SEGG, celebrada los dias 11 y 12 de noviembre y patrocinada por Novartis, reunió en Barcelona a cerca de 50 profesionales para debatir sobre la aproximación diagnóstica a la Enfermedad de Alzheimer (EA) temprana y su abordaje precoz.

Cabe destacar las intervenciones del Dr. Pablo Martinez Laje que resaltó, entre otras aportaciones, el mayor rendimiento diagnóstico del PET y la importancia de la punción lumbar para la determinación de biomarcadores (B-amiloide y Tau), que ya han sido incorporados a los criterios NINCDS–ADRDA revisados (Lancet Neurolol 2007, 6: 734-46)

Diagnostic criteria for AD

Probable AD: A plus one or more supportive features B, C, D, or E

Core diagnostic criteria

A. Presence of an early and significant episodic memory impairment that includes the

following features:

1. Gradual and progressive change in memory function reported by patients or

informants over more than 6 months

2. Objective evidence of signifi cantly impaired episodic memory on testing: this

generally consists of recall defi cit that does not improve signifi cantly or does not

normalise with cueing or recognition testing and after eff ective encoding of

information has been previously controlled

3. The episodic memory impairment can be isolated or associated with other cognitive

changes at the onset of AD or as AD advances

Supportive features

B. Presence of medial temporal lobe atrophy

• Volume loss of hippocampi, entorhinal cortex, amygdala evidenced on MRI with

qualitative ratings using visual scoring (referenced to well characterised population

with age norms) or quantitative volumetry of regions of interest (referenced to well

characterised population with age norms)

C. Abnormal cerebrospinal fluid biomarker

• Low amyloid β1–42 concentrations, increased total tau concentrations, or increased

phospho-tau concentrations, or combinations of the three

• Other well validated markers to be discovered in the future

D. Specifi c pattern on functional neuroimaging with PET

• Reduced glucose metabolism in bilateral temporal parietal regions

• Other well validated ligands, including those that foreseeably will emerge such as

Pittsburg compound B or FDDNP

E. Proven AD autosomal dominant mutation within the immediate family

Exclusion criteria

History

• Sudden onset

• Early occurrence of the following symptoms: gait disturbances, seizures,

behavioural changes

Clinical features

• Focal neurological features including hemiparesis, sensory loss, visual field

deficits

• Early extrapyramidal signs

Other medical disorders severe enough to account for memory and related symptoms

• Non-AD dementia

• Major depression

• Cerebrovascular disease

• Toxic and metabolic abnormalities, all of which may require specifi c

investigations

• MRI FLAIR or T2 signal abnormalities in the medial temporal lobe that are

consistent with infectious or vascular insults

Criteria for definite AD

AD is considered definite if the following are present:

• Both clinical and histopathological (brain biopsy or autopsy) evidence of the

disease, as required by the NIA-Reagan criteria for the post-mortem diagnosis of

AD; criteria must both be present139

• Both clinical and genetic evidence (mutation on chromosome 1, 14, or 21) of AD;

criteria must both be present

El Dr. Jose Luis Molinuevo remarcó la importancia de los biomarcadores B-amiloide y Tau en LCR y su correlación con la cognición. En GDS 3 y GDS 4 los niveles de Tau aumentan y los de B-amiloide disminuyen en LCR; pero incluso en fase preclínica (GDS 1 y 2), cuando todavía la cognición es normal, un porcentaje de personas asintomáticas de riesgo presentan disminución del B-amiloide.

Resaltó también que se detecta un aumento del grosor cortical 15-20 años antes de la fase clínica de la EA en aquellas áreas cerebrales que posteriormente se atrofiarán, lo que también puede ser indicativo de la necesidad de seguimiento clínico.

La neuropsicóloga Miriam Barandiarain explicó la importancia de medir la memoria. Existe disminución de los rendimientios cognitivos (tanto mnésicos como en otras áreas) aproximadamente 10 años antes de la fase clínica de la EA. Es de destacar como las alteraciones de la función visuespacial son detectables hasta 3 años antes del diagnostico de EA. En este sentido resulta recomendable el seguimiento de la memoria, especialmente la episódica, de la función ejecutiva, de la fluidez verbal y de la visuopercepción.