PubMed · 5296333
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G Schubert. 1965-10-25. [Visual cortex and binocular vision].. https://doi.org/10.1007/bf02464810
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DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.
There are distinct qualitative differences between the dementias that present with and without posterior cortical features. These can be utilized in dementia assessment. This paper reviews the validity and potential utility of a dichotomy based on generalized cortical (Type 1) versus isolated frontal system pathology (Type 2). These syndromes are associated with distinct differentials and problem behaviors. They may also result in different caregiving burdens or treatment responses. Alzheimer's disease (AD) is by far the most common cause of the Type 1 syndrome. Type 2 presentations select for potentially reversible non-AD conditions. Common cognitive screening instruments are insensitive to Type 2 cases. However, the Type 1/Type 2 distinction can be made reliably using qualitative clinical rating scales. We will review these instruments and discuss their application in clinical settings.
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