I am trying to check the ameliorative effect of a local substance on AD induced experimental animals, but I cannot do the stereological infusion of STZ or using GE animals.
If you are focusing on cognition enhancement, scopolamine-induced amnesia model is generally used for AD drug discovery. If you are more intrested in neuroprotection, it may not appropriate. How about amyloid beta infusion? Same problem as in STZ?
I also work on rodent model of AD. I infuse oligomeric abeta (1-42) in rat brain steriotaxically and develop the model. you can try this model, it works petty good..
. best of luck with your experiment.
These models are "quick & dirty" and a waste of time and effort ...
the AD field is now even speeding past estavblished amyloid & tau (combination) transgenic mice as AD-models, because they are based on and thereby model EOFAD (at best ...) and do not faithfully recapitulate the genetic and epigenetic complexity of sporadic AD, which for that matter might come in as many flavors as there are patients ...
hope this article will help you a lot
http://www.sciencedirect.com/science/article/pii/S1740675705000563#
To everyone, thank you for the contributions. The fear is in my country of residence research interest is low and there are no tools to work with, any collaborator will be appreciated and a promise of diligence is assured.
We induced AD-like pathology and behaviour thorugh a protocol of Chronic mild stress (CMS) in wild-type-micein mice
http://www.sciencedirect.com/science/article/pii/S0166432811000301
In the following article they use a cell permeable peptide to disrupt the interaction between the alpha-secretase ADAM10 and SAP97. They obtain a model with AD-like pathology (ABeta + Tau + behaviour)
Hope it will help
"Blocking ADAM10 synaptic trafficking generates a model of sporadic Alzheimer’s disease"Epis R et al. Brain 2010: 133; 3323-3335
thank you prof Perez-Mediavilla, but i could not download the material can you please send to my mail ([email protected]). i found some valuable in the article DR Romain.
Dear Balogun, I think that you are a little mechanistic in terms of relating AD in humans and mice or rats. First, what do you want to study? AD is a multifaceted subject.
As regards the cause of AD, the increased oxidative stress looks as the major pathogenic mechanism. I would suggest, that chronic intoxication of animals with barbiturates (using small doses) would be a related model. I think that for the current population of elderly patients with AD, the usage of sleep-well-pills was , probably, one of the causes. In 60s and 70 sleeping drugs were based on barbiturates. Barbiturates are inhibitors of Complex I, and thus similar to rotenone dramatically enhance production of ROS.
@ DR Alexander Panov, I was not trying to be mechanistic instead sir i am realistic, i intend to develop a model of AD in which there is problem with two important protein (APP and PS1) which have been implicated in AD. my plan is to do two things, study the mechanism and develop a therapeutic drug from a herb which have been reported to cure all diseases. i will really love that we talk about it more. i am not targeting oxidative stress nor complex 1 of the respiratory chain.
No longer believe my eyes on what I read here ...
if oxidatve stress is the cause of AD, why does it take 6-8 decades to hit ?
and how does APP & PS1 fit in ?
Regarding animal models for AD I refer to my comment above and to the comment that Hugo Geerts left on LinkedIn just an hour ago
http://www.linkedin.com/groups?viewMemberFeed=&gid=2484646&memberID=15916541
Yes, Fred, beleive it or not, oxidative stress is the major killer of neurons.
I also was wondering what APP & PS1 have to do with AD. It is indeed difficult sometimes to distinguish between the cause and consequences. But a good model of a is always useful to have.
I appreciate the discussion in this thread and would like to add that AD-research is in dire need of novel ideas and out-of-the-box thinking. While the focus on amyloid as a major pathogenetic factor of AD was (and still is) certainly legitimate, being totally exclusive about it in the past 2-3 decades has thrown back the entire field of clinical AD research: virtually all therapeutic approaches to target amyloid (via gamma secretase inhibitors or via antibodies etc), have been effective in animal models but turned out as ineffective and partly even detrimental in AD patients. Just remember some of the recently failed phase III trials on semagacestate and on other agents.
I agree with the notion that neither genetic (amyloid/tau) nor lesion models can sufficiently "simulate" the complex pathophysiology of AD in humans (save perhaps for the ADAD cases caused by distinct mutations). However, that does not preclude that such models can still be very useful to study certain aspects of AD pathophysiology. Genetic models have considerably contributed to our understanding of various aspects of amyloid-beta and tau metabolism. However, where these models fail is to explain AD as a disease. In other words: amyloid and/or tau and/or lesion models do NOT represent the Alzheimer's disase as an entity that we know in humans, but only certain pathophysiological pathways that can also be found in AD.
I think it is important to always have these considerations in mind, when developing or working with animal models.
Please look into the paper: Yehuda and Rabinovitz, (2014), Olfactory bulbectomy as a putative model for Alzheimer': The protective role of essential fatty acids,PharmaNutrition, 2, 12-18,
Dear Yehuda, I am interested in the above mentioned paper but cannot find it from Pubmed? Could you give a bit more detailed info? Thanks!
Dear Tokay
Here us the Abstract. Please send me your email address and I will send you the paper. Best Wishes
-Absract
While the removal of the rat's olfactory bulb considered a valid animal model of depression, recently studies found that those rats exhibited an increase in the hyperphosphorylation of brain Tau proteins and in the number of tangles . The present study investigated the possibility of using rat's olfactory bulbectomy s as a putative model for Alzheimer’s disease. Olfactory bulbectomy indeed mimics a complex of Alzheimer’s symptoms. We evaluated the effect of pretreatment with a specific mixture of omega-3/omega-6 fatty acids: After olfactory bulbectomy, the rats were cognitive impaired, hyperactive, anorectic, and hyperthermic and expressed increased levels of homocysteine and pro-inflammatory cytokines, including IL-17A. Pretreatment with a specific mixture of omega-3/omega-6 fatty acids blocked these adverse effects. We recommend using this model to scan potential new anti-Alzheimer’s drugs and to investigate the role of fatty acids in Alzheimer’s disease.
Shlomo yehuda ,
sir, can you please sent me the mentioned paper . My mail id is [email protected]
Shlomo yehuda,
please i will also like to have the paper, i didnot find it online. Inbox me sir
Scopolamine has been used for inducing short term memory loss in rat models. I was asking in that context. Whether a high dose of scopolamine will produce a permanent memory loss or a prolonged dementia.
@Alok Nahata, scopolamine can only induce amnesia and result into memory loss but cannot induce AD because it cannot cause amyloid beta proteins, neurofibrillary tangles and other features of AD. i hope i answered the question. even the memory, AD memory loss can either be short term or long term but scopolamine will cause loss of long term memory. scopolamine wont do
Long back people used to use AF64A to induce cholinergic neuron loss. I still see some recent papers (PMID: 19941937) using it. Thanks!
@Fred: See http://www.ncbi.nlm.nih.gov/pubmed/10910361 and http://www.ncbi.nlm.nih.gov/pubmed/12867663 . Simple, cumulative cell death due to insult can account for the long incubation of the disease. But, in general, I agree and don't accept the ROS hypothesis either. If increased ROS was the issue in situ we should have seen neurodegeneration in experiments like this one (http://www.ncbi.nlm.nih.gov/pubmed/17895430 ) instead of increased lifespan. While ROS is probably playing a role it is unlikely to be the single biggest factor.
With respect to Alzheimer's disease it is clearly a disease of multiple etiologies and no single mechanism of induction will accurately represent the multiple diseases we refer to as Alzheimer's disease. That being said, NFTs seem to be more critical to brain function than plaques and are common to all Alzheimers-type dementias so any method that will induce NFTs could serve as a useful model provided that all you were doing was looking for ways to stop or reverse NFT development. My little model organism (http://www.ncbi.nlm.nih.gov/pubmed/16461283 ) would appear to spontaneously develop NFTs as well as show cognitive problems with age. What is more, we have wild-type, slow aging, strains for comparison.
This is a very good discussion, it well said that AD is a complex degenerative disorder, managing amylopathies and tauopathies have yielded little or no benefit to the patients. Like someone said we need to think out of the box. possibly brain transport mechanism for example ABCC1 transporter
@Tyrone: txs for the support and the summing-up what AD is: a conglomerate of age-related issues with the same post-mortem outcome of amyloid & tau-tangles !
individual genetic make-up must account for some, but by far not everything - which brings in epigenetics & environment & lifestyle - explaining some of the variability among AD-patients, which is not enough appreciated in the ethiology and in the trials (stratification) -
ROS is part of it, and so is inflammation, but these are present in every (ageing) brain and do not explain the incidence in some - and not in its twin brother for example ... which brings us back to square #1: describe the patients in more detail !
Check out the aluminum model by Judie Walton. In aged rats, aluminum gives a very profound cognitive decline and some of the AD pathology.
@dr shaw thank you for the info, i have tried to check it out but could not find the link, can you send me the link please
There are many neurotoxins used as a tool to study AD pathology.
Their targets are likes oxidative stress and glucose metabolism by STZ.
MAP protein by Colchicine's.
Ca++ by Kainic acid,
Cholinergic neuron by AF64,
Muscarinic cholinergic receptor by Scopolamine,
Okadaic acid by tau hyperphosphorylation and PP2A inhibition.
Few years ago I did some research in AD, and I opted for the aluminium model. I also coudn't use GE or streptozotocin.
I used the protocole for inducing toxicity from the publications 1,2 and the dosage of AlCl3 solution based on publication 3.
1. Sethi P., Jyouti A., Singh R., Hussain E., Sharma D., Aluminium – induces electrophysiological, biochemical and cognitive modifications in the hippocampus of aging rats, NeuroToxicology 29, 2008, 1069-1079
2. Sethi P., Jyuti A., Hussain E., Sharma D., Curcumin attenuates aluminium – induced functional neurotoxicity in rats, Pharmacology, Biochemistry and Behavior 90, 2009, 31-39
3. Kumar S., Acute toxicity of aluminium chloride, acephate, and their coexposure in male Wistar rat, International journal of toxicology 20, 2001, 219-223
Also you could check out Walton J.R., An aluminum-based rat model for Alzheimer’s disease exhibit oxidative damage, inhibition of PP2A activity, hyperphosphorilated tau, and granulovacuolar degeneration, Journal of Inorganic Biochemistry 101, 2007, 1275-1284. This is just one of the papers by Walton J.R, there are lots.
Hope this helps :)
once more - and final as it appears futile:
do not waste any time and resources on this type of models that are simply imposing some sort of toxicity -
remember: "neurons can die in a thousand different ways, and only one is relevant for alzheimer ... "
Alzheimer disease (AD) is only one of many neurodegenerative diseases (NDs), and like most of them is closely related to aging and associated metabolic changes, which are generalized under the name of “Metabolic syndrome”. All animal models have a drawback that you can reproduce some of the symptoms in usually only species. Even transgenic models with mutated human genes strongly depend on the metabolic background of animals. So of particular importance for understanding AD its origin and the way of treatment, is to understand the pathogenic mechanisms of the disease, which we do not know. Amyloid and other similar staff is just consequences, not the cause.
A huge breakthrough in understanding of NDs, and AD in particular, was the discovery of the nonenzymatic auto oxidation of PUFA with the formation of isoprostanes and isoketals. This mechanism has many distinctions from the “classical” lipid peroxidation of PUFA< which is initiated by the hydroxyl radical (OH*). The major initiator of the “isoprostane pathway” of lipid peroxidation is perhydroxyl radical (HO2), which is a protonated form of the superoxide radical.
So, read the latest papers on these subjects, plus “old” papers by Bielski whose works for some reason were neglected, and you will be at the really leading trend of research on NDs. It is also important that you have understand the brain’s metabolism, brain mitochondria in particular? Because they are the major source of SOR and HO2.
Other researchers have indicated already that your toxic model is obsolete because it has nothing to do with the pathogenic mechanisms of AD. Try toxic model with low doses of phenobarbital, which causes chronic increase in production SOR in the brain.
PS. I have attached some of the papers for you to start to read on the subject.
Good luck.
Alexander Panov
You may search for induction using AlCl3.6H2O in young rodents
So does anyone know BCCAO(bilateral common artery cartoid artery occlusion) model of rodent? i practice this to make vascular dementia model. i just wanted to find out what is difference with Scopolamine model and BCCAO model. and now i am here.
then i know that scopolamine is short term memory loss. does anyone try BCCAO model? and why this model is not prefferd?
Jung Lim, BCCAO is a model for ischemic stroke while scopolamine is a model for amnesia.
Well, you may use Aluminium chloride.
https://www.ncbi.nlm.nih.gov/pubmed/25613582
https://www.ncbi.nlm.nih.gov/pubmed/25630717
https://www.hindawi.com/journals/bn/2015/210169/
http://www.sciencedirect.com/science/article/pii/S1995764514602467
https://www.google.com.ng/url?sa=t&rct=j&q=&esrc=s&source=web&cd=8&cad=rja&uact=8&ved=0ahUKEwie9qGy2tzQAhUID8AKHe89DRYQFghPMAc&url=http%3A%2F%2Fresearchpub.org%2Fjournal%2Fand%2Fnumber%2Fvol1-no1%2Fvol1-no1-3.pdf&usg=AFQjCNF4W2rAnK9DPz7PiAnao3wP7kwrJw&bvm=bv.139782543,d.ZGg
https://www.google.com.ng/url?sa=t&rct=j&q=&esrc=s&source=web&cd=4&cad=rja&uact=8&ved=0ahUKEwie9qGy2tzQAhUID8AKHe89DRYQFggzMAM&url=http%3A%2F%2Fmaxwellsci.com%2Fprint%2Fcrjbs%2Fv3-509-515.pdf&usg=AFQjCNH7PVhArLq70nkkKAPzr1enpsSrTQ&bvm=bv.139782543,d.ZGg
Or better still use zebra fish
In case it has not been mentioned so far: the streptozotocine model of AD resembles quite a few core pathological features of AD, including (but not limited to) tau protein pathology, cholinergic and cognitive deficits, and neurodegeneration.
It appears to be a more "complete" model of AD in rodents compared e.g. to transgenic mice with amyloid pathology and it seems to relate better to sporadic AD than to heritable / genetic variants.
For recent review see: J Neural Transm (Vienna). 2013 Jan;120(1):233-52.
https://www.ncbi.nlm.nih.gov/pubmed/22886150
Please suggest what are best method for induction of Alzheimer's disease in wister rats
Please refrain from generating & using animal models with "induced" alzheimer as they are irrelevant - even transgenic models fail to replicate essential features of sporadic AD. The "overdose" at ADPD 2017 of models - new or old or even older - that test for the umpteenth time the same compounds, drugs, treatments with the same methods of analysis & tests and with mostly insufficient numbers/power/statistics ... going in circles - poignant & dire!
Once, when I was working on Alzheimer patients lymphoblastoid cell mitochondria, I was thinking why there was kind of epidemic of the Alzheimer disease among Americans born in 20s of the last century. During 40-60s the common sleeping pills were drugs based on barbiturates/ Barbiturates are inhibitors of Co-I and thus increase production of ROS during sleep. Thus, regular usage of the sleeping drugs at that time might increase the possibility of Alzheimer's disease. But this kind of reaction is highly individual. I used to work with the rotenone model of Parkinson's disease, and found that one week poisoning with low doses of rotenone cause damages to brain mitochondria i all animals? but after 4 weeks of poisoning (using osmotic pump) 8-9 animals showed no decrease in respiration with pyruvate or glutamate. Ranchita Betarbet admitted that histologically only 1-2 animals showed signs of Parkisonism out of 10 poisoned with rotenone for 4 weeks. I have found that most animals after 4 weeks of poisoning started oxidize pyruvate and glutamate via the transamination pathway. Animal models are very very tricky. Example? I was impressed, when I learned, that the only mouse model of hypertension caused by injections of angiotensine work only on C57Bl/6J mice. which lack the important mitochondrial enzyme transhydrogenase.
To come back on animal models. It looks like for some of the more complex processes of neurodegeneration small animal models the 'timing' of biology seems to be different from humans (metabolic rate, induction of gene expression etc.).
Also, coming back to Rotenone, I come to think of it as more of a trigger to start a cascade that is 'ready to go' and could also be started/activated by other suitable factors.
Such as, using your example, Barbiturates, who could also prime/sensitize the system for triggers. Or, if the concentration is really high, start the cascade by themselves.
- Try Judy Walton's method using aluminum compounds in the water of old rats. Seems to work in her hands quite well.
Is carrageenan suitable for the induction of chronic neuro- inflammation in rats,and if the use of Aluminium chloride is the alternative option,what should be the amount of a dose,route of administration? Also for how many hours/days neuroinfammation might last in a tested rat model?
Dementia like symptoms could be induced by different chemicals like streptozotocin treatment augmented by oral administration of Aluminium Chloride 1g/1L for the period of 4 to 6 weeks. Streptozotocin could only be induced by Intraperitoneal injection.
AD is a humaan disease of old age. The marker of AD is not only the loss of neurons in the cortex, but also formation of amiloid, which is the result of the oxidatively damaged proteins. These proteins are damaged by the isoprostane pathway of lipid peroxidation (IPLP), which produces a large number of different compounds such as isoketals, isolevglnadins, etc. The radical, which initiates IPLP is perhydroxyl radical, a protonated superoxide radical. From this mechanism, animal models of AD are mechanistic and irrelevent to the human AD.
@ Waleed Hashmi Hello! Mr. Hashmi can you provide reference for AD induction through oral administration of STZ + Aluminium Chloride? I have found an article about AlCl3 administration but not for both of the above-stated compounds. Thank you
Same way Dr. Walton does it. Seems to work great in older rat's.
Every chemical used will only address the disease mechanisms caused through that chemical.
Last time I looked, very few Alzheimer's cases in humans can be traced back to heavy metals or synthetic toxins.
From the published methods using chemical inducers, I think the bacterial endotoxin models in older rats may come the closest to the general mechanism at play, as the role of bacteria in neuroinflammation is getting more 'popular'.
But the best model will be a transgenic animal that does display a combination of as of now unknown triggers.
.
I have read about the link between Aluminium in food and water and the development of Alzheimer's dementia. Any leads?
Already article published on Aluminum based Alzheimer model:
Article An aluminum-based rat model for Alzheimer’s disease exhibits...
below review paper highlight alzheimer model
https://www.sciencedirect.com/science/article/abs/pii/S0024320514005165?via%3Dihub
One of the good idea for selection model is that which pathway working ....
if work is on inflammation then go with LPS based,
if work on amyloid beta then go with Aβ infusion induced memory deficits
which one is best till date doubt full.. Suggestion from my side if good money for project then go with multiple Transgenic animal models (in sort select beta amyloid, tau based).
Streptozotocin based model work on oxidative stress..
Just look what is purpose of development of model and what is pathway explore
suggestion welcome
allow me to repeat my post dd 24.02.2014 - not much has changed...
These "models" are "quick & dirty" and a waste of time and effort ...
the AD field is now even speeding past established amyloid & tau (combination) transgenic mice as AD-models, because they are based on and thereby model EOFAD (at best ...) and do not faithfully recapitulate the genetic and epigenetic complexity of sporadic AD, which for that matter might come in as many flavors as there are patients !
I completely agree with Dr. Van Leuven. These "models" are too far from reality. One, out of many, problem is that before histological appearance of amyloid, the real cause of AD lies in the dysfunctions of the astroglial-neuronal-microglial system associated with both functional (neurological) and metabolic disturbances. Most of which are purely human.
Dear Wasiu, how would you determine in mice or rats dementia? When you put before yourself a scientific goal, you MUST be very, very specific and critical. First of all AD and dementia in humans are phenomena caused by aging, and age-associated factors include far too many factors. So far, even the well-known rotenone-model off Parkinson disease can be reliably (histologically proved) reproduced on one out of 10-20 animals and only one species. Exactly like in humans. Most research of this kind reproduces not a disease, but responses on the toxin.
Dear Prabhat Upadhyay,
please do not name the usage of scopolamine as a model off AD. That is not correct.
allow me to repeat my post dd 24.02.2014 already reposted on 05.03.2021 - as nothing has changed my views:
These "models" (c.q. chemicals and/or heavy metals) are "quick & dirty" and a waste of time and effort ...
the AD field is now even speeding past established amyloid & tau (combination) transgenic mice as AD-models, because they are based on and thereby model EOFAD (at best ...) and do not faithfully recapitulate the genetic and epigenetic complexity of sporadic AD, which for that matter might come in as many flavors as there are patients !
In my view, the aluminum-based model of AD in rats by Walton seems to work.
Pendergass et sl 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
Pendergass et al., 1997 reproduced all (all) of the hallmark signs of AD but forcing animals to inhale elemental mercury vapor which clearly points toward dentistry. FDA warns that those with neurological diseases should avoid new mercury fillings but correctly warns about removal. IAOMT has a safer protocol.
How to induce AD in PC 12 cell lines of mice, rat please tell me about the drug/agent other than amyloid beta.
Contact
Dr. Nibaldo Inestroza
He is an expert on the matter.
Good luck
Lots of things damage brain but only elemental mercury vapor reproduces all of the biochemical signals penddrgrass 1997
Lots of things damage brain but only elemental mercury vapor reproduces all of the biochemical signals penddrgrass 1997
Lots of things damage brain but only elemental mercury vapor reproduces all of the biochemical signals penddrgrass 1997
Lots of things damage brain but only elemental mercury vapor reproduces all of the biochemical signals penddrgrass 1997
Lots of things damage brain but only elemental mercury vapor reproduces all of the biochemical signals penddrgrass 1997
Lots of things damage brain but only elemental mercury vapor reproduces all of the biochemical signals penddrgrass 1997
Lots of things damage brain but only elemental mercury vapor reproduces all of the biochemical signals penddrgrass 1997
Dear Wasiu Gbolahan Balogun thank you very much for your important technical question. For a good overview on chemicals used to induce Alzheimer's disease in animals please have a look at the following relevant article:
Chemicals used for the induction of Alzheimer’s disease-like cognitive dysfunctions in rodents
http://www.bmrat.org/index.php/BMRAT/article/view/575
This paper has been published Open Access and can be freely downloaded from the general internet. I apologize if this link has been posted before on this thread (I did not check all previous answers).
Also please go through the following relevant RG link:
Drugs Induced Alzheimer's Disease in Animal Model
Article Drugs Induced Alzheimer's Disease in Animal Model
Dear Wasiu Gbolahan Balogun, yes there are some chemicals that can be used to mimic some aspect of Alzheimer's disease. @Frank T Eldelmann, has recommended one of our manuscript to you. You can as well check this on : "https://doi.org/10.1016/j.biopha.2018.04.152". Thanks.
I don't know, nor do I want to know, because I confess that I don't like at all, not at all, certain experiments done on animals, no matter how worthy the intentions of the researchers/scientists may be.
If you do not want tu use such substanzes... feed them with normal drinking water and/or fast food (or food from a normal warehouse with lot of sugar)...if you lay your mobile phone beside them...you will truely have sucess!
cfr below I repeat myself once more ... and for the last time
as I stop following this rather "deaf-scientist society" !
Such models are "quick & dirty" and a waste of time and effort ...
the AD field is speeding up and past "established" amyloid & tau (combination) transgenic mice as AD-models, because they are based on and thereby model (at best some aspects of) mutations leading to EOFAD (early onset AD)
even transgenic models do not faithfully approach, let alone recapitulate, the genetic and epigenetic complexity of sporadic AD, which comes in different forms in different patients ...
You can apply this method. It is highly cited and reliable method. Long-term D-galactose injection combined with ovariectomy serves as a new rodent model for Alzheimer's disease
Xiangdong Hua 1, Ming Lei, Yongjie Zhang, Jiong Ding, Qunying Han, Gang Hu, Ming Xiao
Affiliations expand
PMID: 17391708 DOI: 10.1016/j.lfs.2007.02.030
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