Alteration in the pattern of nerve terminal protein immunoreactivity in the perforant pathway in Alzheimer's disease and in rats after entorhinal lesions

Cabalka, Leanne M.; Hyman, Bradley T.; Goodlett, Charles R.; Ritchie, Teresa C.; Hoesen, Gary W. Van

doi:10.1016/0197-4580(92)90041-u

Cited by 59 publications

(21 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Moreover, because we observe these synaptic changes in a component of hippocampal circuitry associated with spatial memory processing (Morris, 1981;Nagahara et al, 1992) and that these synaptic abnormalities occur at postinjury time intervals when spatial memory showed large deficits, our results strongly suggest that synaptic pathology can be linked with functional outcome when TBI neuroexcitation is followed by hippocampal deafferentation. This conclusion is in agreement with two prior studies, one examining synaptophysin during UEC lesion-induced reactive synaptogenesis (Masliah et al, 1991) and the other during EC degeneration in Alzheimer's disease (Calbaka et al, 1992). Each study found that loss and/or recovery of presynaptic terminals was temporally correlated with both synaptophysin immunobinding and degree of functional recovery.…”

Section: Discussionsupporting

confidence: 89%

Combined Fluid Percussion Brain Injury and Entorhinal Cortical Lesion: A Model for Assessing the Interaction Between Neuroexcitation and Deafferentation

Phillips

Lyeth

Hamm

et al. 1994

Journal of Neurotrauma

View full text Add to dashboard Cite

Laboratory studies suggest that excessive neuroexcitation and deafferentation contribute to long-term morbidity following human head injury. Because no current animal model of traumatic brain injury (TBI) has been shown to combine excessive neuroexcitation and significant levels of deafferentation, we developed a rat model combining the neuroexcitation of fluid percussion TBI with subsequent entorhinal cortical (EC) deafferentation. In this paradigm, moderate fluid percussion TBI was induced in each rat, followed 24 h later by bilateral EC lesion (BEC). Six conditions were examined: (1) fluid percussion TBI followed 24 h later by bilateral EC lesion (TBEC), (2) fluid percussion TBI (TBI), (3) bilateral EC lesion (BEC), (4) sham fluid percussion TBI (SHAM), (5) TBI followed 24 h later by unilateral EC lesion (TUEC), and (6) unilateral EC lesion (UEC). The first four groups were assessed for motor (with beam-balance and beam-walk testing) and cognitive deficits (with the Morris water maze) and hippocampal morphology (with immunocytochemistry and electron microscopy). The TUEC and UEC groups were assessed for cognitive deficits alone. Motor deficits were greater in the TBEC injury than in TBI or sham alone; however, no significant difference was observed between the TBEC and BEC conditions in motor performance. Cognitive deficits were of a greater magnitude in the combined TBEC injury model relative to each individual insult. These cognitive deficits appeared to be additive for the two experimental injuries, BEC deafferentation producing deficits intermediate between TBI and TBEC insults. Morphologic analysis of the dentate gyrus molecular layer at 15 days after TBEC showed that the distribution of synaptophysin-positive presynaptic terminals was distinct from that observed after either TBI or BEC alone. Specifically, the laminar pattern of presynaptic rearrangement induced by BEC lesion did not occur after TBEC injury. The present results show that axonal injury and its attendant deafferentation, when coupled with traumatically induced neuroexcitation, produce an enhancement of the morbidity associated with TBI. Moreover, they indicate that this model can effectively be used to study the interaction between neuroexcitation and synaptic plasticity.

show abstract

Section: Discussionsupporting

confidence: 89%

Combined Fluid Percussion Brain Injury and Entorhinal Cortical Lesion: A Model for Assessing the Interaction Between Neuroexcitation and Deafferentation

Phillips

Lyeth

Hamm

et al. 1994

Journal of Neurotrauma

View full text Add to dashboard Cite

show abstract

“…Synaptic degeneration is also a variable in AD and several studies have demonstrated decreases in the number of synapses [1, 37, 47], and decreases in synaptic proteins (i.e. synaptophysin) [11, 24, 45] in hippocampus and entorhinal cortex in AD, notably early in disease progression. Some evidence suggests that decreases in synaptic density occur after age 65 [38] and others have demonstrated a correlation between dystrophic neurites and severity of dementia [6, 45].…”

Section: Discussionmentioning

confidence: 99%

Entorhinal verrucae geometry is coincident and correlates with Alzheimer’s lesions: a combined neuropathology and high-resolution ex vivo MRI analysis

et al. 2011

View full text Add to dashboard Cite

Entorhinal cortex displays a distinctive organization in layer II and forms small elevations on its surface called entorhinal verrucae. In Alzheimer’s disease, the verrucae disappear due to neurofibrillary tangle formation and neuronal death. Isosurface models were reconstructed from high resolution ex vivo MRI volumes scanned at 7.0 T and individual verruca were measured quantitatively for height, width, volume, and surface area on control and mild Alzheimer’s cases. Mean verruca height was 0.13 ± 0.04 mm for our cognitively normal (controls) sample set whereas for mild AD samples mean height was 0.11 mm ± 0.05 mm (p < 0.001) in entorhinal cortex (n=10 cases). These quantitative methods were validated by a significant correlation of verrucae height and volume with qualitative verrucae ratings (n=36 cases). Entorhinal surfaces were significantly different from other cortical heights such as, cingulate, frontal, occipital, parietal and temporal cortices. Colocalization of verrucae with entorhinal islands was confirmed in ex vivo MRI and, moreover, verrucae ratings were negatively correlated to Braak and Braak pathological stage. This study characterizes novel methods to measure individual entorhinal verruca size, and shows that verrucae size correlates to Alzheimer’s pathology. Taken together, these results suggest that verrucae may have the potential to serve as an early and specific morphological marker for mild cognitive impairment and Alzheimer’s disease.

show abstract

“…neocortical synapses (Cabalka et al 1992;Brown et al 1998). Moreover, mice transgenic for mutated APP or PS1 exhibit severe cognitive deficiency with senile plaques in the brain, but without neuronal loss and neurofibrillary tangles Chapman et al 1999;Dewachter et al 2000).…”

mentioning

confidence: 99%

β‐Amyloid peptide induces formation of actin stress fibers through p38 mitogen‐activated protein kinase

Song

Perides

Wang

et al. 2002

Journal of Neurochemistry

View full text Add to dashboard Cite

Based on the critical role of actin in the maintenance of synaptic function, we examined whether expression of familial b-amyloid precursor protein APP-V642I (IAPP) or mutant presenilin-1 L286V (mPS1) affects actin polymerization in rat septal neuronal cells. Expression of either IAPP or mPS1 but not wild-type amyloid precursor protein or presenilin-1 induced formation of actin stress fibers in SN1 cells, a septal neuronal cell line. Treatment with b-amyloid (Ab) peptide also caused formation of actin stress fibers in SN1 cells and primary cultured hippocampal neurons. Treatment with a c-secretase inhibitor completely blocked formation of actin stress fibers, indicating that overproduction of Ab peptide induces actin stress fibers. Because activation of the p38 mitogen-activated protein kinase (p38MAPK)-mitogen-associated protein kinase-associated protein kinase (MAPKAPK)-2-heat-shock protein 27 signaling pathway mediates actin polymerization, we explored whether Ab peptide activates p38MAPK and MAPKAPK-2. Expression of IAPP or mPS1 induced activation of p38MAPK and MAPKAPK-2. Treatment with a p38MAPK inhibitor completely inhibited formation of actin stress fibers mediated by Ab peptide, IAPP or mPS1. Moreover, treatment with a c-secretase inhibitor completely blocked activation of p38MAPK and MAP-KAPK-2. In summary, our data suggest that overproduction of Ab peptide induces formation of actin stress fibers through activation of the p38MAPK signaling pathway in septal neuronal cells. Keywords: actin stress fibers, Alzheimer's disease, b-amyloid precursor protein, presenilin-1, p38 mitogen-activated protein kinase, mitogen-associated protein kinase-associated protein kinase.

show abstract

Alteration in the pattern of nerve terminal protein immunoreactivity in the perforant pathway in Alzheimer's disease and in rats after entorhinal lesions

Cited by 59 publications

References 45 publications

Combined Fluid Percussion Brain Injury and Entorhinal Cortical Lesion: A Model for Assessing the Interaction Between Neuroexcitation and Deafferentation

Combined Fluid Percussion Brain Injury and Entorhinal Cortical Lesion: A Model for Assessing the Interaction Between Neuroexcitation and Deafferentation

Entorhinal verrucae geometry is coincident and correlates with Alzheimer’s lesions: a combined neuropathology and high-resolution ex vivo MRI analysis

β‐Amyloid peptide induces formation of actin stress fibers through p38 mitogen‐activated protein kinase

Contact Info

Product

Resources

About