scholarly journals A novel hinge system and incubation chamber for emulsion-coated coverslip autoradiography.

1993 ◽  
Vol 41 (9) ◽  
pp. 1419-1427 ◽  
Author(s):  
K J Rhodes ◽  
K A Meiners ◽  
D L Rosene
Keyword(s):  
Alzheimer Disease ◽  
Human Brain ◽  
Tissue Section ◽  
Aluminum Foil ◽  
Immunocytochemical Staining ◽  
Neurotransmitter Receptors ◽  
Neuritic Plaques ◽  
Reagent Solution ◽  
Incubation Chamber ◽  
Autoradiographic Technique

We describe an emulsion-coated coverslip autoradiographic technique for large (50 x 50 mm) sections of monkey or human brain. The technique uses adhesive-backed, teflon-reinforced aluminum foil as a flexible hinge that allows the coverslip to swing away from the slide so that the emulsion and tissue can be processed independently. We also describe a plexiglas incubation chamber that allows two slides with coverslips folded away to be processed back-to-back in 5 ml of reagent solution. In general use, the chamber minimizes the volume of solution needed to cover large slide-mounted sections and is ideal for radioligand or immunohistochemical reactions that use expensive reagents. For autoradiography, the chamber greatly facilitates independent processing of the emulsion and tissue section. Together, the foil-hinge method and incubation chamber virtually eliminate the major technical pitfalls of previous emulsion-coated coverslip methods. Moreover, they facilitate combination of histochemical or immunocytochemical staining with autoradiographic localization of neurotransmitter receptors in the same tissue section. This is demonstrated by thioflavin S staining of neuritic plaques and tangles and autoradiographic localization of serotonin 1A receptors in sections of Alzheimer disease brain.

Cystatin a-like immunoreactivity is widely distributed in human brain and accumulates in neuritic plaques of alzheimer disease subjects

1994 ◽  
Vol 33 (5) ◽  
pp. 477-481 ◽  
Author(s):  
Hans-Gert Bernstein ◽  
Riitta Rinne ◽  
Heidrun Kirschke ◽  
Mikko Järvinen ◽  
Brigitte Knöfelh ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Human Brain ◽  
Neuritic Plaques ◽  
Cystatin A

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.

scholarly journals Strategies for the Identification of Novel Brain Specific Genes Affected in Alzheimer Disease

1989 ◽  
Vol 16 (S4) ◽  
pp. 483-489 ◽  
Author(s):  
D.G. Walker ◽  
B.E. Boyes ◽  
P.L. McGeer ◽  
E.G. McGeer
Keyword(s):  
Alzheimer Disease ◽  
Normal Cell ◽  
Temporal Cortex ◽  
Neuronal Loss ◽  
Brain Regions ◽  
Neuritic Plaques ◽  
Substantia Innominata ◽  
Expression Of Genes ◽  
Preliminary Description ◽  
Specific Mrna

ABSTRACT:The pathological changes that occur in Alzheimer disease (AD) brain lead to a large loss of various classes of neurons and the production of novel proteinaceous elements such as neuritic plaques and neurofibrillary tangles. For the neuronal loss to occur and these elements to arise, there must be a disturbance in the expression or regulation of genes that code for proteins required for normal cell maintenance, or perhaps even for the expression of genes unique to AD. We describe the construction of a cDNA library from the human substantia innominata and strategies for isolating genes that are expressed differentially between brain regions and which may be affected by AD. Some of the results obtained using these strategies and a preliminary description of a novel brain specific mRNA of 15.5kb, whose expression is increased in AD affected temporal cortex, are presented.

scholarly journals A brief history of “Alzheimer disease”

Neurology ◽  
2019 ◽  
Vol 92 (22) ◽  
pp. 1053-1059 ◽  
Author(s):  
David S. Knopman ◽  
Ronald C. Petersen ◽  
Clifford R. Jack
Keyword(s):  
Alzheimer Disease ◽  
Neurofibrillary Tangles ◽  
Public Awareness ◽  
Clinical Status ◽  
Later Life ◽  
Population Based ◽  
Imaging Biomarkers ◽  
Neuritic Plaques ◽  
Β Amyloid ◽  
Definition Of

The field of Alzheimer disease (AD) has a nosologic problem: The diagnostic label “Alzheimer disease” has several distinctive meanings. The term probable AD was introduced in 1984 to designate a clinically diagnosed acquired and progressive amnestic dementia for which there was no evidence for another etiology. Probable AD represented a clinicopathologic entity that assumed a specific and sensitive linkage between amnestic dementia and the neuropathology of β-amyloid-containing neuritic plaques and tau-containing neurofibrillary tangles. The clinicopathologic model represented by probable AD was adapted in abbreviated form for population-based studies and general clinical practice, although the uncertainty connoted by “probable” was often overlooked. Representing the growing public awareness of later life cognitive impairment, a vernacular meaning of AD arose out of the clinicopathologic model in which AD represented all dementia not due to another clinically apparent cause. In contrast, by the 1990s, neuropathologists settled on a definition of AD based entirely on a sufficient burden of neuritic plaques and neurofibrillary tangles at postmortem examination, regardless of antemortem clinical status. In the last decade, the availability of fluid and imaging biomarkers that measure β-amyloid and tau abnormalities has enabled antemortem pathobiological diagnoses, highlighting the divide between the clinicopathologic model, the vernacular usage, and the pathobiological models. Each definition has value. However, the meanings of AD as defined by each of these models are not interchangeable. The pathobiological one is the only one that is unambiguous.

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