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Aging Neurosci."],"abstract":"<jats:p>Cerebellar hypoplasia is a major characteristic of the Down syndrome (DS) brain. However, the consequences of trisomy upon cerebellar Purkinje cells (PC) and interneurons in DS are unclear. The present study performed a quantitative and qualitative analysis of cerebellar neurons immunostained with antibodies against calbindin D-28k (Calb), parvalbumin (Parv), and calretinin (Calr), phosphorylated and non-phosphorylated intermediate neurofilaments (SMI-34 and SMI-32), and high (TrkA) and low (p75<jats:sup>NTR<\/jats:sup>) affinity nerve growth factor (NGF) receptors as well as tau and amyloid in DS (<jats:italic>n<\/jats:italic> = 12), Alzheimer's disease (AD) (<jats:italic>n<\/jats:italic> = 10), and healthy non-dementia control (HC) (<jats:italic>n<\/jats:italic> = 8) cases. Our findings revealed higher A\u03b2<jats:sub>42<\/jats:sub> plaque load in DS compared to AD and HC but no differences in APP\/A\u03b2 plaque load between HC, AD, and DS. The cerebellar cortex neither displayed A\u03b2<jats:sub>40<\/jats:sub> containing plaques nor pathologic phosphorylated tau in any of the cases examined. The number and optical density (OD) measurements of Calb immunoreactive (-ir) PC soma and dendrites were similar between groups, while the number of PCs positive for Parv and SMI-32 were significantly reduced in AD and DS compared to HC. By contrast, the number of SMI-34-ir PC dystrophic axonal swellings, termed torpedoes, was significantly greater in AD compared to DS. No differences in SMI-32- and Parv-ir PC OD measurements were observed between groups. Conversely, total number of Parv- (stellate\/basket) and Calr (Lugaro, brush, and Golgi)-positive interneurons were significantly reduced in DS compared to AD and HC. A strong negative correlation was found between counts for Parv-ir interneurons, Calr-ir Golgi and brush cells, and A\u03b2<jats:sub>42<\/jats:sub> plaque load. Number of TrkA and p75<jats:sup>NTR<\/jats:sup> positive PCs were reduced in AD compared to HC. These findings suggest that disturbances in calcium binding proteins play a critical role in cerebellar neuronal dysfunction in adults with DS.<\/jats:p>","DOI":"10.3389\/fnagi.2021.645334","type":"journal-article","created":{"date-parts":[[2021,3,12]],"date-time":"2021-03-12T08:51:50Z","timestamp":1615539110000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":17,"title":["Cerebellar Calcium-Binding Protein and Neurotrophin Receptor Defects in Down Syndrome and Alzheimer's Disease"],"prefix":"10.3389","volume":"13","author":[{"given":"Jennifer C.","family":"Miguel","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvia E.","family":"Perez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Malek-Ahmadi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elliott J.","family":"Mufson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,3,12]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"297","DOI":"10.1002\/ana.410170313","article-title":"Atypical Alzheimer's disease with spastic paresis and ataxia","volume":"17","author":"Aikawa","year":"1985","journal-title":"Ann. 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