Saiz-Sanchez Daniel, De la Rosa-Prieto Carlos, Ubeda-Banon Isabel, Martinez-Marcos Alino
Laboratorio de Neuroplasticidad y Neurodegeneración, Facultad de Medicina de Ciudad Real, Centro Regional de Investigaciones Biomédicas, Universidad de Castilla-La Mancha, Avda. de Moledores s/n, 13071, Ciudad Real, Spain.
Brain Struct Funct. 2015 Jul;220(4):2011-25. doi: 10.1007/s00429-014-0771-3. Epub 2014 Apr 19.
Impaired olfaction has been described as an early symptom of Alzheimer's disease. Neuroanatomical changes underlying this deficit in the olfactory system are largely unknown. Interestingly, neuropathology begins in the transentorhinal cortex and extends to the neighboring limbic system and basal telencephalic structures that mediate olfactory processing, including the anterior olfactory nucleus and olfactory bulb. The human piriform cortex has been described as a crucial area in odor quality coding; disruption of this region mediates early olfactory deficits in Alzheimer's disease. Most neuropathological investigations have focused on the entorhinal cortex and hippocampus, whereas the piriform cortex has largely been neglected. This work aims to characterize the expression of the neuropathological amyloid-β peptide, tau protein and interneuron population markers (calretinin, parvalbumin and somatostatin) in the piriform cortex of ten Alzheimer-diagnosed (80.4 ± 8.3 years old) and five control (69.6 ± 11.1) cases. Here, we examined the distribution of different interneuronal markers as well as co-localization of interneurons and pathological markers. Results indicated preferential vulnerability of somatostatin- (p = 0.0001 < α = 0.05) and calretinin-positive (p = 0.013 < α = 0.05) cells that colocalized with amyloid-β peptide, while the prevalence of parvalbumin-positive cells was increased (p = 0.045 < α = 0.05) in the Alzheimer's cases. These data may help to reveal the neural basis of olfactory deficits linked to Alzheimer's disease as well as to characterize neuronal populations preferentially vulnerable to neuropathology in regions critically involved in early stages of the disease.
嗅觉减退被认为是阿尔茨海默病的早期症状。嗅觉系统中导致这种缺陷的神经解剖学变化在很大程度上尚不清楚。有趣的是，神经病理学始于内嗅皮质，并延伸至邻近的边缘系统和基底前脑结构，这些结构介导嗅觉处理，包括前嗅核和嗅球。人类梨状皮质被描述为气味质量编码的关键区域；该区域的破坏介导了阿尔茨海默病早期的嗅觉缺陷。大多数神经病理学研究都集中在内嗅皮质和海马体，而梨状皮质在很大程度上被忽视了。这项工作旨在描述10例被诊断为阿尔茨海默病（80.4±8.3岁）和5例对照（69.6±11.1岁）患者梨状皮质中神经病理学淀粉样β肽、tau蛋白和中间神经元群体标记物（钙视网膜蛋白、小白蛋白和生长抑素）的表达情况。在这里，我们检查了不同中间神经元标记物的分布以及中间神经元与病理标记物的共定位。结果表明，与淀粉样β肽共定位的生长抑素阳性（p = 0.0001 <α = 0.05）和钙视网膜蛋白阳性细胞（p = 0.013 <α = 0.05）存在优先易损性，而在阿尔茨海默病病例中，小白蛋白阳性细胞的患病率增加（p = 0.045 <α = 0.05）。这些数据可能有助于揭示与阿尔茨海默病相关的嗅觉缺陷的神经基础，并确定在该疾病早期关键区域中优先易受神经病理学影响的神经元群体特征。
