Alzheimer's disease (AD) the most common form of dementia is characterized by cognitive decline and progressive loss of neurons in the central nervous system. Despite huge scientific progress, there are only few animal models that recapitulate at least majority of the AD pathology and related symptomatology. Therefore, alternative methods to develop animal models for neurodegenerative diseases are constantly explored. Recently, recombinant adeno-associated viruses (AAVs) are widely used viral vectors in development of novel models for neurodegenerative diseases. AAV vectors expressing full length, mutant or truncated forms of tau demonstrate early and robust pathology characterized by AT8 positivity, NFT formation, motor and cognitive deficits. Furthermore, AAVs have been used in expression of tau in amyloid rodent models thus developing both lesions of amyloid and tau therefore recapitulating AD like features. Major advantage of AAV as a delivery system is the site specific expression of tau, mostly in hippocampus and cortex, and thus elimination of unwanted ectopic transgene expression. These novel models may help in better understanding of AD etiopathogenesis and provide a platform for development and testing of disease modifying drugs in preclinical efficacy studies.
Alzheimer's disease is currently the most common neurodegenerative disorder, characterized by distinct cognitive and sensory deficits. The underlying pathogenetic mechanisms, however, still remain elusive. How the molecular and morphological changes associated with Alzheimer's disease affect information processing in neuronal circuits and translate into cognitive dysfunction is unclear. Inhibitory interneurons have recently emerged as one of the earliest and important culprits in mediating dysfunction of neuronal circuits in neurodegeneration. Amyloid-beta and tau protein have been both linked to interneuron dysfunction, and likely play an important, albeit unknown, role in mediating changes in the overall activity of neuronal circuits. Resolving the role of inhibitory interneurons in neurodegeneration-specific changes in neuronal activity is crucial for understanding the impact of Alzheimer's disease on brain function and even for possible identification of effective treatments and diagnostic techniques (Ref. 63).
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