Filamentous Tau Pathology in Nerve Cells, Astrocytes, and Oligodendrocytes of Aged Baboons

Schultz, Christian; Dehghani, Faramarz; Hubbard, Gene B.; Thal, Dietmar Rudolf; Struckhoff, Gernot; Braak, Eva; Braak, Heiko

doi:10.1093/jnen/59.1.39

Cited by 89 publications

(59 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…(Delacourte et al, 2002(Delacourte et al, , 2003. Recently, several authors reported an age-dependent pattern of glial tau aggregation in both human and baboon brains (Schultz et al, 2000;Yang et al, 2005b). Previous studies have shown that hyperphosphorylation of tau occurs in the brain of SAMP8 mice at 5 months of age (Canudas et al, 2005;Sureda et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Dysfunction of astrocytes in senescence‐accelerated mice SAMP8 reduces their neuroprotective capacity

et al. 2008

View full text Add to dashboard Cite

SummaryEarly onset increases in oxidative stress and tau pathology are present in the brain of senescence-accelerated mice prone (SAMP8). Astrocytes play an essential role, both in determining the brain's susceptibility to oxidative damage and in protecting neurons. In this study, we examine changes in tau phosphorylation, oxidative stress and glutamate uptake in primary cultures of cortical astrocytes from neonatal SAMP8 mice and senescenceaccelerated-resistant mice (SAMR1). We demonstrated an enhancement of abnormally phosphorylated tau in Ser 199 and Ser 396 in SAMP8 astrocytes compared with that of SAMR1 control mice. Gsk3β β β β and Cdk5 kinase activity, which regulate tau phosphorylation, was also increased in SAMP8 astrocytes. Inhibition of Gsk3β β β β by lithium or Cdk5 by roscovitine reduced tau phosphorylation at Ser 396 .Moreover, we detected an increase in radical superoxide generation, which may be responsible for the corresponding increase in lipoperoxidation and protein oxidation. We also observed a reduced mitochondrial membrane potential in SAMP8 mouse astrocytes. Glutamate uptake in astrocytes is a critical neuroprotective mechanism. SAMP8 astrocytes showed a decreased glutamate uptake compared with those of SAMR1 controls. Interestingly, survival of SAMP8 or SAMR1 neurons cocultured with SAMP8 astrocytes was significantly reduced. Our results indicate that alterations in astrocyte cultures from SAMP8 mice are similar to those detected in whole brains of SAMP8 mice at 1-5 months. Moreover, our findings suggest that this in vitro preparation is suitable for studying the molecular and cellular processes underlying early aging in this murine model. In addition, our study supports the contention that astrocytes play a key role in neurodegeneration during the aging process.

show abstract

Section: Discussionmentioning

confidence: 99%

Dysfunction of astrocytes in senescence‐accelerated mice SAMP8 reduces their neuroprotective capacity

et al. 2008

View full text Add to dashboard Cite

show abstract

“…An age-dependent increase in the phosphorylation of TAU and the formation of neurofibrillary tangles has, for example, been observed in aged bears (Cork et al, 1988), sheep, goats (Braak et al, 1994), bison (Härtig et al, 2000), mouse lemurs (Bons et al, 1995), baboons (Schultz et al, 2000) and various other mammals (Härtig et al, 2001).…”

Section: Tau Hyperphosphorylationmentioning

confidence: 99%

Chronic stress as a risk factor for Alzheimer’s disease

Machado¹,

Herrera²,

Pablos³

et al. 2014

Reviews in the Neurosciences

151

View full text Add to dashboard Cite

AbstractThis review aims to point out that chronic stress is able to accelerate the appearance of Alzheimer’s disease (AD), proposing the former as a risk factor for the latter. Firstly, in the introduction we describe some human epidemiological studies pointing out the possibility that chronic stress could increase the incidence, or the rate of appearance of AD. Afterwards, we try to justify these epidemiological results with some experimental data. We have reviewed the experiments studying the effect of various stressors on different features in AD animal models. Moreover, we also point out the data obtained on the effect of chronic stress on some processes that are known to be involved in AD, such as inflammation and glucose metabolism. Later, we relate some of the processes known to be involved in aging and AD, such as accumulation of β-amyloid, TAU hyperphosphorylation, oxidative stress and impairement of mitochondrial function, emphasizing how they are affected by chronic stress/glucocorticoids and comparing with the description made for these processes in AD. All these data support the idea that chronic stress could be considered a risk factor for AD.

show abstract

“…35,63,135,152,160,161 Typically these tau changes tend to be sporadic and do not adopt the full blown features of intracellular NFTs and are usually not associated with neuronal loss. Interestingly, even in nonhuman primates, which display substantial plaques formation and tau proteins with highly conserved amino acid sequences, NFT are rarely observed.…”

Section: Neuronal Lesionsmentioning

confidence: 99%

Pathology of the Aging Brain in Domestic and Laboratory Animals, and Animal Models of Human Neurodegenerative Diseases

et al. 2016

View full text Add to dashboard Cite

According to the WHO, the proportion of people over 60 years is increasing and expected to reach 22% of total world's population in 2050. In parallel, recent animal demographic studies have shown that the life expectancy of pet dogs and cats is increasing. Brain aging is associated not only with molecular and morphological changes but also leads to different degrees of behavioral and cognitive dysfunction. Common age-related brain lesions in humans include brain atrophy, neuronal loss, amyloid plaques, cerebrovascular amyloid angiopathy, vascular mineralization, neurofibrillary tangles, meningeal osseous metaplasia, and accumulation of lipofuscin. In aging humans, the most common neurodegenerative disorder is Alzheimer's disease (AD), which progressively impairs cognition, behavior, and quality of life. Pathologic changes comparable to the lesions of AD are described in several other animal species, although their clinical significance and effect on cognitive function are poorly documented. This review describes the commonly reported age-associated neurologic lesions in domestic and laboratory animals and the relationship of these lesions to cognitive dysfunction. Also described are the comparative interspecies similarities and differences to AD and other human neurodegenerative diseases including Parkinson's disease and progressive supranuclear palsy, and the spontaneous and transgenic animal models of these diseases.

show abstract

Filamentous Tau Pathology in Nerve Cells, Astrocytes, and Oligodendrocytes of Aged Baboons

Cited by 89 publications

References 62 publications

Dysfunction of astrocytes in senescence‐accelerated mice SAMP8 reduces their neuroprotective capacity

Dysfunction of astrocytes in senescence‐accelerated mice SAMP8 reduces their neuroprotective capacity

Chronic stress as a risk factor for Alzheimer’s disease

Pathology of the Aging Brain in Domestic and Laboratory Animals, and Animal Models of Human Neurodegenerative Diseases

Contact Info

Product

Resources

About