Literature: A-K ; L-Z ; subject area
Compiled by: Julian Thorpe
AD and Tauopathy Models
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Please Note: Due to time constraints, the text part of this page has not been updated for some time. However, references are added reasonably frequently. |
latest on: animal models ; beta-amyloid immunization ; References
 | Recent work on transgenic mice (summarised by Mudher and Lovestone, 2002 ) has taken us tantalisingly close to the answer to plaque/tangle inter-relationships. These authors report: |
 | that as (in human brain) "mutations in tau..." (that lead to the FTD disorders) "...give rise to tau-inclusion tangles but not plaques and yet mutations in APP or....presenilin ...give rise to both plaques and tangles almost proves that amyloid pathology occurs upstream of tau pathology " (my italics). |
| I am personally not quite convinced by this latter, but better evidence is... |
| that transgenic mice doubly mutant for mutant APP (the single transgene exhibits only plaques) and tau (the single transgene exhibits only tangles) have more tangles than mice with the single mutant tau transgene and tangles appear in areas of the brain that are unaffected in single mutant-tau transgenic mice ( Lewis et al., 2001) . |
| that amyloid injections also exacerbated tangle pathology in mutant-tau mice (Gotz et al., 2001) . |
| that they suggest that "increasingly the finger points to souluble beta-amyloid as the culprit,.." |
| that it "remains a mystery" why beta-amyloid (injections) does not stimulate tau pathology with wild-type tau (Gotz et al., 2001) , yet other transgenic mice overexpressing wild-type tau exhibit tangles (Ishihara et al., 1999and 2001 ) |
'State of Play' as of 2000 or so:
Quite extensive research has been carried out on animal models of AD , but a significant shortcoming of these models thus far is an absence of a strain exhibiting full NFT development (although early tau pathology has been modelled: Sommer et al., 2000)
"The ongoing combination by breeding with other transgenic mouse strains, i.e. mice over-expressing human Presenilin 1, ApoE 4 and tau to generate "multiple" transgenic mice, offer additional potential to define the pathological interactions of these genetic factors, known to be involved, directly or indirectly, in dementia of the Alzheimer type. Finally, it must be the aim to obtain transgenic mice that not only model amyloidogenesis, but also the neurofibrillary tangle pathology and the involvement of protein tau."(from van Leuven, 2000)
Immunization with Beta-Amyloid
: promising early work, but recent disappointment
| Janus et al. (2000) show that such immunization (in TgCRND8 mice) reduces deposition of fibrillar beta-amyloid but, significantly, also alleviates cognitive impairment. As there was not an overall reduction in total brain beta-amyloid levels, they concluded either: (i) that the partial (c. 50%) clearance of plaques might suffice to produce this improvement; or (ii) that there is a specific effect of immunization upon on a small subpopulation of especially-neurotoxic beta-amyloid. These authors also noted that the alleviation of cognitive loss could be interpreted as being corroboratory to the 'amyloid cascade ' theory of AD pathogenesis. |
| In the same issue of Nature , Morgan et al . (2000) report on a study of a transgenic mouse AD model combining beta-amyloid vaccination with learning performance tests. Their results suggested that such vaccination could not only prevent, but also perhaps treat the deleterious effects of amyloid deposition. The latter conclusion was based upon the observation that vaccinated transgenic mice actually exhibited superior cognitive performances to the control (nontransgenic) animals. |
| In this regard, Bard et al . (2000) have reported in Nature Medicine that this efficacy might be antibody-mediated. Peripherally-administered beta-amyloid antibodies were shown to cross the blood-brain barrier, enter the CNS and bind to, and reduce, amyloid plaques in PDAPP transgenic mice. |
| N.B. Unfortunately, human trials of such beta-amyloid vaccination have been recently halted owing to cerebral inflammation occurring in a number of the volunteers ( see report on the Alzheimer's Research Forum Site) |
Transgenic mice
| Over-expression of mutated human amyloid precursor protein (APP): Masliah et al. (1996) found neurodegenerative changes in mice over expressing an APP (amyloid protein precursor) to be similar to those of AD. Neuritic plaques contained a dense amyloid core, which was surrounded by anti-APP and NF immunoreactive dystrophic neurites and astroglial cells. The dystrophic neurites in plaques of both the transgenic mice and AD tissue contained (many dense multilaminar bodies and) neurofilaments . Apoptotic features were found in the transgenic mice but no paired helical filaments . |
| Expression of a fusion protein composed of NF-H fused to beta-galactosidase (LacZ): Tu et al. (1997) found that transgenic mice expressing a fusion protein composed of NF-H fused to beta-galactosidase developed inclusions in neurons throughout the CNS. These contained massive filamentous aggregates of the endogenous NF proteins and the fusion protein which resembled the NF-rich Lewy bodies of Parkinson's disease and Lewy Body dementia. In hippocampal neurons they found that the inclusions which entrapped organelles (type II) led to neuronal cell death. |
| Neurofilament Effects: Transgenic mice studies have shown evidence that neurofilaments can affect the dynamics and perhaps the function of other cytoskeletal elements, such as microtubules and actin. |
| ApoE knockout mice evidenced dendritic alterations which led to synaptic simplification similar to that seen in AD. |
| Stress-activated protein kinases : Giasson et al. (1997: in transgenic mice) have shown that activation of stress-activated protein kinases (SAPKs) by an upstream activator (MEKK-1) caused extensive NF-H phosphorylation. (Aberrant hyperphosphorylation of perikaryal NF-H [neurofilament heavy chain] is a common feature of many neurological diseases). SAPK was localised in the neurites as well as the cell body and they suggested that it could be involved in the phosphorylation of NF-H in neurites (neuritic NFH is highly-phosphorylated despite a demonstrated absence of cyclin-dependent kinase 5 activity in these neurons). |
| Ahlijanian et al. (2000) used transgenic mice (overexpressing human p25, which activates cdK5 ) to show hyperphosphorylation of tau and neurofilaments by cdk5. This latter was accompanied by cytoskeletal disruption. |
| Bornemann and Staufenbiel (2000) have generated transgenic mouse lines expressing the human amyloid precursor protein (APP). Their model system displayed plaques (with associated heparansulfate proteoglycan and apolipoprotein E ), activated astrocytes and microglia, enlarged dystrophic neurites and hyperphosphorylated tau reminiscent of early tau pathology. Neuronal cell loss in the hippocampus correlated with plaque load. Crossbreeding with transgenic mice carrying AD-linked presenilin mutations enhanced the observed pathology. |
| From their work on transgenic mice, Mucke et al ., 2000 concluded that plaque-independent beta-amyloid toxicity may lead to synaptic deficits in AD and related conditions. |
| Leutner et al. (2000) used transgenic mice with human PS1 mutations to show evidence of a reduction in the activity of two antioxidant enzymes (Cu/Zn superoxide dismutase and glutathione reductase). |
| Capsoni et al. (2000) have published a paper utilising transgenic mice over-expressing a neutralizing anti-nerve growth factor (NGF) recombinant antibody. These mice show an age-dependent formation of amyloid plaques , hyperphosphorylated tau and NFTs in cortical and hippocampal neurons. They state that this model is "the most comprehensive" and that "the overall picture is strikingly reminiscent of human AD". They conclude that (in mice at least) a deficit in the signaling and/or transport of NGF leads to neurodegeneration. |
| Lewis et al (2001) showed that transgenic mice doubly mutant for mutant APP (the single transgene exhibits only plaques) and tau (the single transgene exhibits only tangles) have more tangles than mice with the single mutant tau transgene and tangles appear in areas of the brain that are unaffected in single mutant-tau transgenic mice. |
| Gotz et al (2001) reportedthat amyloid injections exacerbated tangle pathology in mutant-tau but not wild-type tau transgenic mice. |
| Ishihara et al (1999 and 2001 ) found that transgenic mice overexpressing wild-type tau exhibited tangles. |
| Carter et al. (2001) have shown that human ApoE4 accelerates beta-amyloid deposition in APPsw transgenic mouse brain. |
Pig Model of Diffuse Brain Injury
| Brain trauma increases the risk of AD in humans. Smith et al. (1999) have used a pig model of diffuse brain injury and they found beta-amyloid and tau accumulations. These latter co-localised with immunoreactive beta-amyloid precursor protein and NF in damaged axons throughout the white matter of all injured animals (after 3-10 days). In some animals diffuse beta-amyloid plaques were found in grey and white matter and tau accumulations and NF-rich inclusions were observed in neuronal perikarya. |
| Model of Aluminium Neurotoxicity: Strong et al. (1994) used rabbits to test the effects of aluminium neurotoxicity and found that NF-L and NF-M messenger RNA levels were reduced in direct proportion to the extent of NF inclusion formation. |
| A rabbit model exhibiting plaques, NFTs (and oxidative stress) in the hippocampushas been produced by treatment with aluminium (Rao et al., 2000) . |
| Cerebral explants to test aluminium/glutamate effects: Using rat cerebral explants, Jones et al. (1998) examined the effects of aluminium and glutamate upon PHF formation. Found that aluminium could cause significant accumulations of curved filaments but only one of the samples looked at had possibly PHF-like filaments. The authors suggested that postulations of a link between aluminium and AD might be premature. |
| Experimental autoimmune dementia (EAD): The work of Oron et al. (1997) suggests a role for serum antibodies (against phosphorylated epitopes highly enriched in the heavy neurofilament protein NF-H) in the neurodegeneration of cholinergic neurons in AD. |
| E.g. Fath et al. (2001), Feany (2000) |
| And see review by Link (2001) |
| E.g. Feany (2000), Gunawardena and Goldstein (2001) , Wittmann et al. (2001) |
| And see reviews by Chan and Bonini (2000) and Link (2001) |
| Jackson et al. (2002) have shown that human wild-type tau interacts with wingless pathway components to produce neurofibrillary pathology in Drosophila. |
| Imahori and Uchida (1997 ) have shown, using primary cultures of embryonic rat hippocampus, that beta-amyloid treatment induced GSK-3 beta kinase activity, extensive phosphorylation of tau and cell death. GSK-3 beta interacted with pyruvate dehydrogenase (PDH), thereby reducing levels of acetyl-CoA, essential for acetylcholine synthesis. |
| Alvarez et al. (1999) used cultured rat hippocampal cells to study the tau protein kinase II system (TPK II; involving cdk5 and p35). They showed that fibrillary beta-amyloid increased cdk5 activity, while a cdk5 inhibitor and an (cdk5) antisense probe protected the cells from beta-amyloid-induced neurotoxic damage. They therefore concluded that cdk5 plays a major role in the molecular path leading to the neurodegenerative process. |
| Niikura et al. (2000) have used neuronal cells which can inducibly express the amyloid protein precursor (APP). They found that the cells expressing APP became apoptotic. |
| Ray et al. (2000) have used PC12 cells to show that the upregulation of calpain (a Ca2+-dependent cysteine protease) by oxidative stress and calcium influx, resulted in NF-L degradation (and apoptosis). |
| Gibson et al. (2000) have used cultured fibroblasts to study a-ketoglutarate dehydrogenase complex (KGDHC; a key mitochondrial enzyme whose activity is reduced in AD brain). KGDHC was shown to be sensitive to oxidative stress (in cells, purified mitochondria and as an isolated protein) and their results were suggested to be indicative of the enzyme's involvement in critical events related to oxidative stress-induced selective neuronal loss. |
| Armogida et al. (2001) have used presenilin -deficient embryonic mouse fibroblasts to show that the production of endogenous secreted and intracellular 40- and 42-amino-acid A beta peptides is unaffected. However, presenilin deficiency did abolish the release of the Notch intracellular domain (NICD) from Notch. Their data thus showed, that in murine fibroblasts at least, NICD production is presenilin-dependent and that there is a gamma-secretase activity distinct from presenilin. |
| Perez et al (2002) used okadaic acid and hydroxynonenal (a product of oxidative stress) to stimulate the in vitro formation of aggregates of phospho-tau protein in SH-SY5Y cells. They suggest that both phosphorylation of tau oxidative modification is required for tau filament formation. |
| Ljungberg et al. (2002) have shown that truncated apoE forms tangle -like structures in a neuronal cell line. |
(These journals include: Neurology, Neurobiology of Disease, Journal of Neurochemistry, Alzheimer's Disease Review)
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