Transgenic models of Alzheimer’s disease: Learning from animals

Spires, Tara L.; Hyman, Bradley T.

doi:10.1602/neurorx.2.3.423

Cited by 186 publications

(142 citation statements)

References 190 publications

(182 reference statements)

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“…Хорошо известно, что генетические/эпигенетические и средовые факторы являются триггерами событий, актуальных для патогенеза болезни Альцгеймера. Ис-следования, выполненные в течение 2-3 последних десятилетий, в основном были сосредоточены на изу-чении роли генетических факторов, что нашло свое отражение не только в идентификации новых генов-кандидатов, но и в создании трансгенных моделей бо-лезни Альцгеймера на животных [42]. Однако в течение последних 5-10 лет все большее внимание исследова-телей привлекает изучение действия факторов окружа-ющей среды на формирование хронического нейроде-генеративного процесса как в клинической практике, так и у животных с экспериментальными моделями бо-лезни Альцгеймера [43].…”

Section: влияние обогащенной среды на поврежденный мозг: возможности unclassified

Changes in Structural and Functional Plasticity of the Brain Induced by Environmental Enrichment

IuK

et al. 2013

ARAMS

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The review contains current data on structural and functional brain plasticity mechanisms under the enriched environment. Enriched environment contains social and non-social stimuli acting on different aspects of the development and functioning of the brain. Special attention is devoted to the Влияние факторов внешней среды на развитие и функционирование головного мозгаГоловной мозг млекопитающих формируется путем реализации сложных генетических и эпигенетических программ. Тем не менее сенсорная, когнитивная и мо-торная стимуляция через взаимодействие с окружающей средой от рождения до старости играет ключевую роль в образовании нейронных цепей, необходимых для нор-мального функционирования мозга. В течение последних десятилетий были детально изучены генетические и фар-макологические факторы, модулирующие функции мозга и его дисфункцию, тогда как средовым параметрам было уделено гораздо меньше внимания [1].

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Section: влияние обогащенной среды на поврежденный мозг: возможности unclassified

Changes in Structural and Functional Plasticity of the Brain Induced by Environmental Enrichment

IuK

et al. 2013

ARAMS

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“…49,50 These models recapitulate various aspects of AD and frontal temporal lobe dementia and are inherently useful for understanding the timing of neurogenetic changes in AD progression. Such studies have so far produced conflicting results showing increases, 51 non-significant changes, 52 and decreases 53 in hippocampal neurogenesis in mouse models that depend, in part, on methodological differences in markers for neurogenesis and the age of the animals.…”

Section: Future Directionsmentioning

confidence: 99%

Alzheimer’s Disease and Adult Neurogenesis—Are Endogenous Stem Cells Part of the Solution?

Marlatt¹,

Hoozemans²,

Veerhuis³

et al. 2009

US Neurology

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Numerous clinical trials are under way to evaluate therapeutic approaches to stop the progression of Alzheimer's disease (AD).Despite the significant efforts toward, for example, clearance of amyloid plaques by vaccination therapies, these approaches may still fall short of cognitive recovery in the AD population as they do not directly focus on the regeneration of damaged tissue and restoration of brain function. Adult neurogenesis is a unique form of structural plasticity in the brain that has important implications in hippocampaldependent learning and behavior. While not shown to have direct links with AD, adult neurogenesis is carefully regulated by various factors, including ones that affect AD, and should be evaluated independently and in relation to Alzheimer's pathology. AbstractThe human brain produces new neurons that mediate hippocampal plasticity but also have a potential role in hippocampal-related disorders, such as Alzheimer's disease and dementia. Factors such as stress and aging that reduce adult neurogenesis also serve as independent risk factors for Alzheimer's disease. Causality between loss of neurogenesis and hippocampal dysfunction has not been established; however, neurogenesis is an attractive research avenue for therapy since it is readily modifiable. Activities such as running and enrichment increase the proliferation of neural stem cells and survival of nascent neuroblasts. Adult neurogenesis may alternatively reflect capacity to overcome age-dependent insults and neurodegeneration in the hippocampus. This collectively indicates that stimulation of endogenous cells or transplantation of neural stem cells are potential pathways reversing the behavioral changes associated with neurodegenerative disorders by augmenting structural plasticity of the hippocampus. Continued research in this area and in appropriate animal models of disease is critical for evaluating whether neurogenesis-based therapeutic strategies will have the potential to aid those with degenerative conditions.

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“…In addition, although studies of knockout mice suggested that APP was not an essential protein [114], all the cleavage products of APP, including the large soluble N-terminus, Aβ and the C-terminus, have been shown to have physiological roles [28]. Thus, inhibition of β-or γ-secretase may interfere with physiological processes and cause significant adverse side effects [110,115].…”

Section: New Therapeutic Strategiesmentioning

confidence: 99%

Early diagnostics and therapeutics for Alzheimer’s disease – how early can we get there?

Monien¹,

Apostolova²,

Bitan³

2006

Expert Review of Neurotherapeutics

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Alzheimer's disease (AD) is a major threat for the rapidly aging world population. AD is the leading cause of dementia and a major cause of death in developed countries. The disease puts a tremendous practical, emotional and financial burden on individuals and governments. Clinicians and researchers in the AD field face great challenges: the pathophysiological processes that cause AD are not well understood, definite diagnosis of AD requires autopsy, and therapeutic options are limited to treating the symptoms rather than the cause of the disease. Nevertheless, new insights into the earliest events that lead to development of AD increase hope that reliable diagnostics and efficacious therapies may emerge. KeywordsAβ; Alzheimer's disease; amyloid; dementia; diagnosis; mild cognitive impairment; therapy Alzheimer's disease (AD) is the most common form of late-life dementia, accounting for approximately two-thirds of all dementia cases [1]. AD is a major cause of death and a tremendous financial and emotional problem, the magnitude of which is predicted to increase steeply in the next few decades if no cure is found. Here, we review the current knowledge of the processes that lead to AD and their implications on recent advances in diagnostics and therapeutics for AD. To this end, we have chosen a stepwise approach of increasing complexity in each step. We discuss how molecular events affect cells, cellular insults accumulate into tissue damage and tissue deterioration eventually affects the whole person. This stepwise approach is directed at both clinicians and basic researchers working in the AD field. †Author for correspondence,

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Transgenic models of Alzheimer’s disease: Learning from animals

Cited by 186 publications

References 190 publications

Changes in Structural and Functional Plasticity of the Brain Induced by Environmental Enrichment

Changes in Structural and Functional Plasticity of the Brain Induced by Environmental Enrichment

Alzheimer’s Disease and Adult Neurogenesis—Are Endogenous Stem Cells Part of the Solution?

Early diagnostics and therapeutics for Alzheimer’s disease – how early can we get there?

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