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A new insight on Al-maltolate-treated aged rabbit as Alzheimer's animal model.
Brain Res Rev. 2006 Sep; 52(2):275-92.BR

Abstract

Lack of an adequate animal model for Alzheimer's disease (AD) has limited an understanding of the pathogenesis of the disease and the development of therapeutic agents targeting key pathophysiological processes. There are undoubtedly few satisfactory animal models for exploring therapies targeting at amyloid beta (Abeta) secretion, deposition, aggregation, and probably the inflammatory response. However, an understanding of the complex events--tau, Abeta, oxidative stress, redox active iron, etc.--involved in the neuronal cell loss is still unclear due to the lack of a suitable animal model system. The use of neurotoxic agents particularly aluminum-organic complexes, especially Al-maltolate, expands the scope of AD research by providing new animal models exhibiting neurodegenerative processes relevant to AD neuropathology. Examination of different species of aged animals including the rapidly advancing transgenic mouse models revealed very limited AD-like pathology. Most other animal models have single event expression such as extracellular Abeta deposition, intraneuronal neurofilamentous aggregation of proteins akin to neurofibrillary tangles, oxidative stress or apoptosis. To date, there are no paradigms of any animal in which all the features of AD were evident. However, the intravenous injection of Al-maltolate into aged New zealand white rabbits results in conditions which mimics a number of neuropathological, biochemical and behavioral changes observed in AD. Such neurodegenerative effects include the formation of intraneuronal neurofilamentous aggregates that are tau positive, immunopositivity of Abeta, presence of redox active iron, oxidative stress and apoptosis, adds credence to the value of this animal model system. The use of this animal model should not be confused with the ongoing controversy regarding the possible role of Al in the neuropathogenesis, a debate which by no means has been concluded. Above all this animal model involving neuropathology induced by Al-maltolate provides a new information in understanding the mechanism of neurodegeneration.

Authors+Show Affiliations

Department of Biochemistry and Nutrition, Central Food Technological Research Institute, Mysore-570013, India.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

16782202

Citation

Bharathi, , et al. "A New Insight On Al-maltolate-treated Aged Rabbit as Alzheimer's Animal Model." Brain Research Reviews, vol. 52, no. 2, 2006, pp. 275-92.
Bharathi , Shamasundar NM, Sathyanarayana Rao TS, et al. A new insight on Al-maltolate-treated aged rabbit as Alzheimer's animal model. Brain Res Rev. 2006;52(2):275-92.
Bharathi, ., Shamasundar, N. M., Sathyanarayana Rao, T. S., Dhanunjaya Naidu, M., Ravid, R., & Rao, K. S. (2006). A new insight on Al-maltolate-treated aged rabbit as Alzheimer's animal model. Brain Research Reviews, 52(2), 275-92.
Bharathi , et al. A New Insight On Al-maltolate-treated Aged Rabbit as Alzheimer's Animal Model. Brain Res Rev. 2006;52(2):275-92. PubMed PMID: 16782202.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A new insight on Al-maltolate-treated aged rabbit as Alzheimer's animal model. AU - Bharathi,, AU - Shamasundar,N M, AU - Sathyanarayana Rao,T S, AU - Dhanunjaya Naidu,M, AU - Ravid,R, AU - Rao,K S J, Y1 - 2006/06/16/ PY - 2005/08/07/received PY - 2006/03/31/revised PY - 2006/04/04/accepted PY - 2006/6/20/pubmed PY - 2006/11/15/medline PY - 2006/6/20/entrez SP - 275 EP - 92 JF - Brain research reviews JO - Brain Res Rev VL - 52 IS - 2 N2 - Lack of an adequate animal model for Alzheimer's disease (AD) has limited an understanding of the pathogenesis of the disease and the development of therapeutic agents targeting key pathophysiological processes. There are undoubtedly few satisfactory animal models for exploring therapies targeting at amyloid beta (Abeta) secretion, deposition, aggregation, and probably the inflammatory response. However, an understanding of the complex events--tau, Abeta, oxidative stress, redox active iron, etc.--involved in the neuronal cell loss is still unclear due to the lack of a suitable animal model system. The use of neurotoxic agents particularly aluminum-organic complexes, especially Al-maltolate, expands the scope of AD research by providing new animal models exhibiting neurodegenerative processes relevant to AD neuropathology. Examination of different species of aged animals including the rapidly advancing transgenic mouse models revealed very limited AD-like pathology. Most other animal models have single event expression such as extracellular Abeta deposition, intraneuronal neurofilamentous aggregation of proteins akin to neurofibrillary tangles, oxidative stress or apoptosis. To date, there are no paradigms of any animal in which all the features of AD were evident. However, the intravenous injection of Al-maltolate into aged New zealand white rabbits results in conditions which mimics a number of neuropathological, biochemical and behavioral changes observed in AD. Such neurodegenerative effects include the formation of intraneuronal neurofilamentous aggregates that are tau positive, immunopositivity of Abeta, presence of redox active iron, oxidative stress and apoptosis, adds credence to the value of this animal model system. The use of this animal model should not be confused with the ongoing controversy regarding the possible role of Al in the neuropathogenesis, a debate which by no means has been concluded. Above all this animal model involving neuropathology induced by Al-maltolate provides a new information in understanding the mechanism of neurodegeneration. SN - 0165-0173 UR - https://www.unboundmedicine.com/medline/citation/16782202/A_new_insight_on_Al_maltolate_treated_aged_rabbit_as_Alzheimer's_animal_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0165-0173(06)00015-4 DB - PRIME DP - Unbound Medicine ER -