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Abstract
Adult hippocampal neurogenesis (AHN) has been widely confirmed in mammalian brains. A growing body of evidence points to the fact that AHN sustains hippocampal-dependent functions such as learning and memory. Impaired AHN has been reported in post-mortem human brain hippocampus of Alzheimer's disease (AD) and is considered to contribute to defects in learning and memory. Neurofibrillary tangles (NFTs) and amyloid plaques are the two key neuropathological hallmarks of AD. NFTs are composed of abnormal tau proteins accumulating in many brain areas during the progression of the disease, including in the hippocampus. The physiological role of tau and impact of tau pathology on AHN is still poorly understood. Modifications in AHN have also been reported in some tau transgenic and tau-deleted mouse models. We present here a brief review of advances in the relationship between development of tau pathology and AHN in AD and what insights have been gained from studies in tau mouse models.
Highlights
Alzheimer’s disease (AD) has two neuropathological hallmarks, amyloid plaques, and Neurofibrillary tangles (NFTs)
Afferent pathways to the dentate gyrus (DG) are affected by NFTs developing in the entorhinal cortex [6], and NFTs develop in the granule cell layer (GCL) [7, 8] in the DG in AD and in some tau transgenic mouse models (Figures 1A–D)
Abnormalities in Adult hippocampal neurogenesis (AHN) have been extensively investigated in AD mouse models based on amyloid precursor protein (APP) or PSEN1/2 familial AD mutations [13, 14], the impact of tau pathology on AHN remains largely unclear in AD and other tauopathies
Summary
AD has two neuropathological hallmarks, amyloid plaques, and NFTs. Amyloid plaques are composed of amyloid ß peptides [1] derived from successive cleavages of amyloid precursor protein (APP) [2]. 3R tau isoform lacking exon 2 and 3 is expressed in the adult brain in the immature neurons in the SGZ [60] and can be used as a specific marker to detect newborn neurons and newly generated axons in the adult mouse hippocampus [28, 61]. The number of cells expressing 3R tau isoforms in the SGZ decreases with age in mice, but they are still detectable at 12 months (Figure 1G) [12].
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