Neurofibrillary tangles, granulovacuolar degeneration, and neuron loss in down syndrome: Quantitative comparison with alzheimer dementia

1980 ◽  
Vol 7 (5) ◽  
pp. 462-465 ◽  
Author(s):  
M. J. Ball ◽  
K. Nuttall
2001 ◽  
Vol 125 (4) ◽  
pp. 489-492 ◽  
Author(s):  
Kymberly A. Gyure ◽  
Robert Durham ◽  
Walter F. Stewart ◽  
John E. Smialek ◽  
Juan C. Troncoso

Abstract Context.—Down syndrome patients who live to middle age invariably develop the neuropathologic features of Alzheimer disease, providing a unique situation in which to study the early and sequential development of these changes. Objective.—To study the development of amyloid deposits, senile plaques, astrocytic and microglial reactions, and neurofibrillary tangles in the brains of young individuals (<30 years of age) with Down syndrome. Methods.—Histologic and immunocytochemical study of a series of autopsy brains (n = 14, from subjects aged 11 months to 56 years, with 9 subjects <30 years) examined at the Office of the Chief Medical Examiner of the State of Maryland and The Johns Hopkins Hospital. Results.—The principal observations included the presence of intraneuronal Aβ immunostaining in the hippocampus and cerebral cortex of very young Down syndrome patients (preceding the extracellular deposition of Aβ) and the formation of senile plaques and neurofibrillary tangles. Conclusions.—We propose the following sequence of events in the development of neuropathologic changes of Alzheimer disease in Down syndrome: (1) intracellular accumulation of Aβ in neurons and astrocytes, (2) deposition of extracellular Aβ and formation of diffuse plaques, and (3) development of neuritic plaques and neurofibrillary tangles with activation of microglial cells.


1990 ◽  
Vol 49 (3) ◽  
pp. 265
Author(s):  
E. H. Bigio ◽  
D. R. Sparkman ◽  
A. W. Clark ◽  
C. L. White

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Kathleen M. Enstice ◽  
Christa L. Hladik ◽  
Ping Shang ◽  
Charles L. White

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Kristen E. Funk ◽  
Jeff Kuret

Alzheimer's disease is characterized pathologically by extracellular senile plaques, intracellular neurofibrillary tangles, and granulovacuolar degeneration. It has been debated whether these hallmark lesions are markers or mediators of disease progression, and numerous paradigms have been proposed to explain the appearance of each lesion individually. However, the unfaltering predictability of these lesions suggests a single pathological nidus central to disease onset and progression. One of the earliest pathologies observed in Alzheimer's disease is endocytic dysfunction. Here we review the recent literature of endocytic dysfunction with particular focus on disrupted lysosomal fusion and propose it as a unifying hypothesis for the three most-studied lesions of Alzheimer's disease.


1987 ◽  
Vol 73 (3) ◽  
pp. 240-246 ◽  
Author(s):  
J. Ulrich ◽  
M. Haugh ◽  
B. H. Anderton ◽  
A. Probst ◽  
C. Lautenschlager ◽  
...  

2015 ◽  
Vol 7 (1) ◽  
Author(s):  
Sally Hunter ◽  
◽  
Thais Minett ◽  
Tuomo Polvikoski ◽  
Elizabeta Mukaetova-Ladinska ◽  
...  

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