Quantitative Analysis of Lipofuscin and Neurofibrillary Tangles in the Hippocampal Neurons of Alzheimer Disease Brains

1994 ◽  
Vol 5 (5) ◽  
pp. 229-233 ◽  
Author(s):  
Alex Stojanovic ◽  
Alex E. Roher ◽  
Melvyn J. Ball
Keyword(s):  
Quantitative Analysis ◽  
Alzheimer Disease ◽  
Neurofibrillary Tangles ◽  
Hippocampal Neurons

Structural and Chemical Studies of Pathological Fibers in Human Neurofibrillary Degeneration

1985 ◽  
Vol 43 ◽  
pp. 726-729
Author(s):  
K.S. Kosik ◽  
L.K. Duffy ◽  
S. Bakalis ◽  
C. Abraham ◽  
D.J. Selkoe
Keyword(s):  
Monoclonal Antibodies ◽  
Alzheimer Disease ◽  
Human Brain ◽  
Neurofibrillary Tangles ◽  
Morphological Analysis ◽  
High Specificity ◽  
Cytoskeletal Proteins ◽  
Neuritic Plaque ◽  
Protein Chemistry ◽  
Chemical Studies

The major structural lesions of the human brain during aging and in Alzheimer disease (AD) are the neurofibrillary tangles (NFT) and the senile (neuritic) plaque. Although these fibrous alterations have been recognized by light microscopists for almost a century, detailed biochemical and morphological analysis of the lesions has been undertaken only recently. Because the intraneuronal deposits in the NFT and the plaque neurites and the extraneuronal amyloid cores of the plaques have a filamentous ultrastructure, the neuronal cytoskeleton has played a prominent role in most pathogenetic hypotheses.The approach of our laboratory toward elucidating the origin of plaques and tangles in AD has been two-fold: the use of analytical protein chemistry to purify and then characterize the pathological fibers comprising the tangles and plaques, and the use of certain monoclonal antibodies to neuronal cytoskeletal proteins that, despite high specificity, cross-react with NFT and thus implicate epitopes of these proteins as constituents of the tangles.

Activation Mechanism of Brain Microglia in Patients With Diffuse Neurofibrillary Tangles With Calcification: A Comparison With Alzheimer Disease

2001 ◽  
Vol 15 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Kazuhiro Imamura ◽  
Makoto Sawada ◽  
Norio Ozaki ◽  
Hiroshi Naito ◽  
Nakao Iwata ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Neurofibrillary Tangles ◽  
Activation Mechanism

Aβ1–42 reduces synapse number and inhibits neurite outgrowth in primary cortical and hippocampal neurons: A quantitative analysis

2008 ◽  
Vol 175 (1) ◽  
pp. 96-103 ◽  
Author(s):  
Nicholas A. Evans ◽  
Laura Facci ◽  
Davina E. Owen ◽  
Peter E. Soden ◽  
Stephen A. Burbidge ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Neurite Outgrowth ◽  
Hippocampal Neurons

scholarly journals Accumulation of Aspartic Acid421- and Glutamic Acid391-Cleaved Tau in Neurofibrillary Tangles Correlates With Progression in Alzheimer Disease

2008 ◽  
Vol 67 (5) ◽  
pp. 470-483 ◽  
Author(s):  
Gustavo Basurto-Islas ◽  
Jose Luna-Muñoz ◽  
Angela L. Guillozet-Bongaarts ◽  
Lester I. Binder ◽  
Raul Mena ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Neurofibrillary Tangles

Fine Tuning of Intracellular Ca2+ Content by Pharmacological Agents – A Strategy to Prevent Synapse Loss in Alzheimer Disease Hippocampal Neurons

2021 ◽  
Vol 17 (12) ◽  
pp. 1065-1071
Author(s):  
Elena Popugaeva
Keyword(s):  
Alzheimer Disease ◽  
Calcium Channels ◽  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Fine Tuning ◽  
Dominant Form ◽  
Pharmacological Agents ◽  
Chemical Structures ◽  
Synapse Loss ◽  
Β Amyloid

: Alzheimer disease is the dominant form of elderly dementia. Today all clinical trials that target β-amyloid have failed to indicate that β-amyloid may not be a causative agent in AD pathogenesis. Thus there is a need to search for alternative ways to treat AD patients. : Neuronal store-operated calcium entry is a fine-tuning mechanism that regulates intracellular Ca2+ content. Recent evidence suggests that store-operated calcium channels may be targeted with pharmacological agents in order to prevent synapse loss, recover long-term potentiation and change behavior. : Current mini-review discusses basic chemical structures that modulate intracellular calcium dysbalance via targeting store-operated calcium channels and their applicability as anti-AD pharmacological agents.

Intraneuronal Aβ-Amyloid Precedes Development of Amyloid Plaques in Down Syndrome

2001 ◽  
Vol 125 (4) ◽  
pp. 489-492 ◽  
Author(s):  
Kymberly A. Gyure ◽  
Robert Durham ◽  
Walter F. Stewart ◽  
John E. Smialek ◽  
Juan C. Troncoso
Keyword(s):  
Down Syndrome ◽  
Alzheimer Disease ◽  
Neurofibrillary Tangles ◽  
Senile Plaques ◽  
Medical Examiner ◽  
Johns Hopkins Hospital ◽  
Sequence Of Events ◽  
Amyloid Deposits ◽  
Aβ Amyloid ◽  
Intraneuronal Aβ

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.

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