Familial influence on plaque formation in the beagle brain

Russell, Michael J.; White, R. G.; Patel, Ela; Markesbery, William R.; Watson, Charles; Geddes, James W.

doi:10.1097/00001756-199212000-00015

Cited by 35 publications

(18 citation statements)

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“…The animals received low levels of strontium-90 in their diet, but their longevity did not significantly differ from those of the control group. A previous study indicated a similar diffuse plaque distribution for this group and for those animals that were not exposed to radiation (33). The beagles either died of natural causes or were euthanized, due to terminal illness or chronic pain.…”

Section: Aged Canine Tissuessupporting

confidence: 67%

“…Aged dogs develop diffuse plaques and rarely exhibit neuritic plaques and neurofibrillary tangles (8,33). Aged bears develop both neuritic (senile) plaques and neurofibrillary tangles (7).…”

Section: 42 43mentioning

confidence: 99%

“…The aged beagle dog brain tissues examined in this study (Table 1) were obtained from the National Radiobiology Archives, as previously described (8,33). The animals received low levels of strontium-90 in their diet, but their longevity did not significantly differ from those of the control group.…”

Section: Aged Canine Tissuesmentioning

confidence: 99%

“…These lesions are also present in the brain of aged mammals including dogs, bears, and primates (7,23,33). In this study, antibodies specific for the carboxy terminal of AI3 were used to compare the deposits present in the aged mammals with those observed in Alzheimer's disease (AD) and in nondemented elderly individuals.…”

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confidence: 99%

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Carboxy terminal of β-amyloid deposits in aged human, canine, and polar bear brains

Tekirian

Cole

Russell

et al. 1996

Neurobiology of Aging

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terminal of ~-amyloid deposits in human, canine, and polar bear brains. NEUROBIOL AGING 17(2) 249-257, 1996.--Immunocytochemistry, using antibodies specific for different carboxy termini of AI340 and AI342(43), was used to compare [3-amyloid deposits in aged animal models to nondemented and demented Alzheimer's disease human cases. Aged beagle dogs exhibit diffuse plaques in the absence of neurofibrillary pathology and the aged polar bear brains contain diffuse plaques and PHF-l-positiw~ neurofibrillary tangles. The brains of nondemented human subjects displayed abundant diffuse plaques, whereas the AD cases had both diffuse and mature (cored) neuritic plaques. Diffuse plaques were positively immunostained with an antibody against A[342(43) in all examined species, whereas AI340 immunopositive mature plaques were observed only in the human brain. Anti-Al~40 strongly immunolabeled cerebrovascular [3-amyloid deposits in each of the species examined, although some deposits in the polar bear brain were preferentially labeled with anti-A[342(43). [3-Amyloid deposition was evident in the outer molecular layer of the dentate gyrus in the aged dog, polar bear, and human. Within this layer, A1342 was present as diffuse deposits, although these deposits were morphologically distinct in each of the examined animal models. In dogs, A[342 was cloud-like in nature; the polar bear demonstrated a more aggregated type of deposition, and the nondemented human displayed well-defined deposits. Alzheimer's disease cases were most frequently marked by neuritic plaques in this region. Taken together, the data indicate that 13-amyloid deposition in aged mammals is similar to the earliest stages observed in human brain. In each species, AI342(43) is the initially deposited isoform in diffuse plaques.

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Section: Aged Canine Tissuessupporting

confidence: 67%

Section: 42 43mentioning

confidence: 99%

Section: Aged Canine Tissuesmentioning

confidence: 99%

mentioning

confidence: 99%

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Carboxy terminal of β-amyloid deposits in aged human, canine, and polar bear brains

Tekirian

Cole

Russell

et al. 1996

Neurobiology of Aging

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“…Senile plaques and the diffuse deposits of Aβ are considered the hallmarks of the aging dog [35,56]. Their presence in association with cognitive decline has led to their being proposed as the major factor implicated in neurodegeneration.…”

Section: Aβ Diffuse Plaque Maturation Aβ Oligomers Neuronal Vulneramentioning

confidence: 99%

Dogs with Cognitive Dysfunction Syndrome: A Natural Model of Alzheimer’s Disease

Bosch¹,

Pugliese²,

Gimeno-Bayón³

et al. 2012

CAR

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In the search for appropriate models for Alzheimer's disease (AD) involving animals other than rodents, several laboratories are working with animals that naturally develop cognitive dysfunction. Among the animals tested, dogs are quite unique in helping to elucidate the cascade of events that take place in brain amyloid-beta (Aβ) deposition aging, and cognitive deficit. Recent innovative research has validated human methods and tools for the analysis of canine neuropathology and has allowed the development of two different approaches to investigate dogs as natural models of AD. The first approach relates AD-like neuropathy with the decline in memory and learning ability in aged housed dogs in a highly controlled laboratory environment. The second approach involves research in family-owned animals with cognitive dysfunction syndrome. In this review, we compare the strengths and limitations of housed and family-owned canine models, and appraise their usefulness for deciphering the early mechanisms of AD and developing innovative therapies.KEYWORDS: aging, Amyloid-beta, animal model, canine cognitive dysfunction syndrome, family dog, therapies. 6 Why a canine model of AD?For years, the search for appropriate animal models for Alzheimer's disease (AD) has focused on a variety of manipulations to reproduce the disease in various species, such as yeast, Drosophyla melanogaster, Caenorabditis elegans, rodents, and rabbits, with a particular interest in obtaining knockout and transgenic animals (for a review, see [1]research is currently performed in the mouse because its brain structure is somewhat similar to that of humans, and it is amenable to highly sophisticated genetic engineering. Because age-related cognitive decline is a common feature of most mammals, other laboratories have focused on the few species that naturally develop cognitive dysfunction with various Alzheimer-like characteristics. These animals include the monkey, polar bear, cat and dog [2][3][4][5]. Canine models are currently considered a useful intermediate between genetically modified mouse models and humans [6,7]. Although many of the transgenic AD models have provided insights into the molecular mechanisms of the pathology, none of them encompass all the cognitive deficits observed in AD (see Table 1). One of the first transgenic mouse AD models was the amyloid precursor protein transgenic mouse, PDAPP mouse, which develops age-dependent amyloid beta accumulation and deposition in both diffuse and fibrillar neuritic plaques in the hippocampus, cerebral cortex, and corpus callosum [8]. Other models with AD-like pathology are apolipoprotein E (ApoE) or Tau transgenic mice, and also mice in which other genes have been modified. In more sophisticated approaches, important information has been gained from crossing PDAPP and ApoE models and with mice lacking or over-expressing genes for beta-secretase, alpha-secretase, or the insulin-degrading enzyme [9,10].All these models have provided valuable information on AD pathology and on the poss...

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Tau hyperphosphorylation in synaptosomes and neuroinflammation are associated with canine cognitive impairment

Smolek

Maďari

Farbáková

et al. 2015

J of Comparative Neurology

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Canine cognitive impairment syndrome (CDS) represents a group of symptoms related to the aging of the canine brain. These changes ultimately lead to a decline of memory function and learning abilities, alteration of social interaction, impairment of normal housetraining, and changes in sleep-wake cycle and general activity. We have clinically examined 215 dogs, 28 of which underwent autopsy. With canine brains, we performed extensive analysis of pathological abnormalities characteristic of human Alzheimer's disease and frontotemporal lobar degeneration, including β-amyloid senile plaques, tau neurofibrillary tangles, and fused in sarcoma (FUS) and TAR DNA-binding protein 43 (TDP43) inclusions. Most demented dogs displayed senile plaques, mainly in the frontal and temporal cortex. Tau neurofibrillary inclusions were found in only one dog. They were identified with antibodies used to detect tau neurofibrillary lesions in the human brain. The inclusions were also positive for Gallyas silver staining. As in humans, they were distributed mainly in the entorhinal cortex, hippocampus, and temporal cortex. On the other hand, FUS and TDP43 aggregates were not present in any of the examined brain samples. We also found that CDS was characterized by the presence of reactive and senescent microglial cells in the frontal cortex. Our transcriptomic study revealed a significant dysregulation of genes involved in neuroinflammation. Finally, we analyzed tau phosphoproteome in the synaptosomes. Proteomic studies revealed a significant increase of hyperphosphorylated tau in synaptosomes of demented dogs compared with nondemented dogs. This study suggests that cognitive decline in dogs is related to the tau synaptic impairment and neuroinflammation. J. Comp. Neurol. 524:874-895, 2016. © 2015 Wiley Periodicals, Inc.

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Familial influence on plaque formation in the beagle brain

Cited by 35 publications

References 0 publications

Carboxy terminal of β-amyloid deposits in aged human, canine, and polar bear brains

Carboxy terminal of β-amyloid deposits in aged human, canine, and polar bear brains

Dogs with Cognitive Dysfunction Syndrome: A Natural Model of Alzheimer’s Disease

Tau hyperphosphorylation in synaptosomes and neuroinflammation are associated with canine cognitive impairment

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