Laminar distribution of neocortical senile plaques in senile dementia of the alzheimer type

Duyckaerts, Charles; Hauw, J. J.; Bastenaire, F.; Piette, F.; Poulain, C.; Rainsard, V.; Javoy‐Agid, F.; Berthaux, P

doi:10.1007/bf00686079

Cited by 147 publications

(60 citation statements)

References 23 publications

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“…This factor may account for the incomplete overlap in distribution between immunodetectable amyloid deposits and silver-stained plaques. Nevertheless, our data agree with those of other groups (20)(21)(22) …”

Section: Methodssupporting

confidence: 93%

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Laminar-specific distribution and infrastructural detail of amyloid in the Alzheimer disease cortex visualized by computer-enhanced imaging of epitopes recognized by monoclonal antibodies.

Majocha

Beneš

Reifel

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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Monoclonal antibodies to the A4 amyloid polypeptide were used in immunocytochemical saining of the Alzheimer disease prefrontal cortex. Analysis of the resulting staining patterns allowed us to evaluate the amounts and distribution of amyloid-protein deposits exclusive of other senile-plaque components. Previously unappreciated infrastructural details of amyloid in the Alzheimer disease brain became accessible through computer-enhanced imaging procedures. Four discrete morphologic classes of amyloid deposits were observed and classified as punctate, macular, ring, and ring-with-core configurations. Computer imaging indicated that all four classes of immunostained deposits contain internal gradients ofdensity. The classes were nonuniformly distributed with regard to size and location within cortical laminae. Our results support two separate but complementary hypotheses concerning the molecular neuropathology of Alzheimer disease in the prefrontal cortex. (i) Irrespective of cortical layer or morphology, density-gradient analyses suggest that amyloid deposits are elaborated through molecular and cellular events that may involve diffusion or coalescence ofthe A4 polypeptide.(it) The distribution and morphology of prefrontal cortical amyloid deposits may be dependent upon underlying laminarspecific structures of the neocortex.Senile plaques, found in abundance in the Alzheimer disease (AD) brain, contain a core with the A4 region of the amyloid precursor (1). Since the A4 cDNA domain cloned from AD brain mRNA has the same structure as that from nondemented brain (2), local cellular mechanisms may be significantly involved in the regulation of amyloid metabolism. In this regard no information is available on the relationship, if any, between discrete brain cytoarchitectural components and plaque size, morphology, or rate of amyloid accumulation. Indeed, the origin of the senile plaque has been a subject of speculation for at least six decades (3, 4).The present report addresses certain of these issues by focusing exclusively upon the A4 amyloid component of senile plaques as revealed by immunologic methods combined with computer-enhanced imaging, rather than traditional silver stains. With the newer approach, we observed unexpected morphologic diversity among amyloid deposits with respect to their size, morphology, internal composition, and laminar distribution. Specimens of prefrontal cortex immunostained for A4 amyloid were examined through a Leitz Laborlux 12 light microscope equipped with an MCI 65 televideo camera that interfaced with an AT&T PC6300 computer. The transmitted images of immunostained amyloid deposits were processed by Bioquant microdensitometry computer software equipped with pseudocolor optical density coding (R&M Biometrics, Nashville, TN). The computer, which perceives the range of optical density as a gray scale, was formatted to distinguish six levels of gray and to express each of these as a different color, as shown by the color bar in Fig. 3. The transmitted image was reconstructed...

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Section: Methodssupporting

confidence: 93%

“…Other workers, using classical staining techniques, observed that layers II and III contain abundant senile plaques, whereas layer I contains the fewest (20)(21)(22). We confirmed these findings with a conventional Bielchowsky silver staining procedure.…”

Section: Methodssupporting

confidence: 88%

Laminar-specific distribution and infrastructural detail of amyloid in the Alzheimer disease cortex visualized by computer-enhanced imaging of epitopes recognized by monoclonal antibodies.

Majocha

Beneš

Reifel

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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“…The find ings indicate that this change occurs in pyramidal neu rons, although other neuronal types may also be affected. These results add to the many studies which have re ported on the distribution of AD-related neuropathologial changes, for example involving neurofibrillary tangles and senile plaques [10,20,31,32,[44][45][46], neuronal loss [10,20,24,26,[47][48][49], tau protein immunoreactivity [50], and acetyl cholinesterase activity [51,52], Although the significance of the present findings in relation to these other studies is unclear, further knowledge of the distribu tion of the various neuropathological correlates of AD may lead to advances in the classification of the demen tias on the basis of pathogenic mechanisms.…”

Section: Discussionsupporting

confidence: 54%

Alzheimers Disease: Distribution of Changes in Intraneuronal Lipopigment in the Frontal Cortex

Dowson

Mountjoy²,

Cairns³

et al. 1995

Dement Geriatr Cogn Disord

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Brains from 22 patients with Alzheimer''s disease (AD) and 20 non-diseased subjects were examined. Intraneuronal lipopigment in 2,440 nucleolated neurons throughout the depth of cortex was identifled by fluorescence microscopy. In the AD brains, the mean total area per neuron of the outlines of lipopigment was significantly increased in the region adjacent to the brain surface (sixths 1-3), and analysis of variance showed a significant interaction between depth of cortex (in sixths) and AD for this lipopigment variable (p = 0.012). After relating this lipopigment variable to the size of neuronal bodies, the results indicate that this change occurs in pyramidal neurons, although other neuronal types may also be affected. At least one of three AD-related changes in lipopigment was found in each sixth of the depth of cortex.

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“…The distribution of the LB, LN, LG together with surviving neurons, EN, vacuoles, and glial cell nuclei was studied from pia mater to white matter using methods described previously [10]. Five traverses from pia mater to the edge of the white matter were located randomly along each gyrus.…”

Section: Morphometric Methodsmentioning

confidence: 99%

Laminar degeneration of frontal and temporal cortex in Parkinson disease dementia

Armstrong

2017

Neurol Sci

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Laminar distribution of neocortical senile plaques in senile dementia of the alzheimer type

Cited by 147 publications

References 23 publications

Laminar-specific distribution and infrastructural detail of amyloid in the Alzheimer disease cortex visualized by computer-enhanced imaging of epitopes recognized by monoclonal antibodies.

Laminar-specific distribution and infrastructural detail of amyloid in the Alzheimer disease cortex visualized by computer-enhanced imaging of epitopes recognized by monoclonal antibodies.

Alzheimers Disease: Distribution of Changes in Intraneuronal Lipopigment in the Frontal Cortex

Laminar degeneration of frontal and temporal cortex in Parkinson disease dementia

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