Featured
-
-
Article |
Modulating TRADD to restore cellular homeostasis and inhibit apoptosis
The adaptor protein TRADD is a regulator of both cellular homeostasis and apoptosis, and represents a potential therapeutic target for human diseases.
- Daichao Xu
- , Heng Zhao
- & Junying Yuan
-
Article |
Restoration of brain circulation and cellular functions hours post-mortem
A specialized technology can restore and preserve microcirculation and cellular functions hours post-mortem in an isolated pig brain.
- Zvonimir Vrselja
- , Stefano G. Daniele
- & Nenad Sestan
-
Letter |
Parkin and PINK1 mitigate STING-induced inflammation
Acute and chronic mitochondrial stress in mice require PINK1 and parkin to restrain STING-mediated innate immunity.
- Danielle A. Sliter
- , Jennifer Martinez
- & Richard J. Youle
-
Article |
Pyramidal cell regulation of interneuron survival sculpts cortical networks
Excitatory input onto inhibitory interneurons in the developing mouse cortex acts through PTEN to protect interneurons from cell death and thus regulate the balance between excitation and inhibition.
- Fong Kuan Wong
- , Kinga Bercsenyi
- & Oscar Marín
-
Letter |
ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy
ApoE4 exacerbates tau pathogenesis, neuroinflammation and tau-mediated neurodegeneration independently of brain amyloid-β pathology, and exerts a ‘toxic’ gain of function whereas its absence is protective.
- Yang Shi
- , Kaoru Yamada
- & David M. Holtzman
-
Letter |
TAM receptors regulate multiple features of microglial physiology
Microglial phagocytosis is required for neurogenic niche maintenance and response to injury; the TAM kinases Mer and Axl are expressed by microglia in the adult CNS, and mediate the clearance of apoptotic cells from the niche.
- Lawrence Fourgeaud
- , Paqui G. Través
- & Greg Lemke
-
Letter |
Aprataxin resolves adenylated RNA–DNA junctions to maintain genome integrity
This study shows that aprataxin, encoded by a gene mutated in the neurodegenerative disorder AOA1, can remove the 5′ AMP from RNA–DNA junctions; this RNA–DNA damage response promotes cell survival.
- Percy Tumbale
- , Jessica S. Williams
- & R. Scott Williams
-
Letter |
Intrinsically determined cell death of developing cortical interneurons
The cell death of inhibitory neurons, which originate far from the cortical areas to which they migrate during embryonic development, is determined autonomously rather than by competition for trophic signals from other cell types.
- Derek G. Southwell
- , Mercedes F. Paredes
- & Arturo Alvarez-Buylla
-
Article |
Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not
Neurons of the peripheral nervous system need survival factors to prevent their death during development. Most in the central nervous system do not. Why are peripheral neurons so needy? Here it is shown that the neurotrophin receptors TrkA and TrkC, expressed at high levels by many peripheral nervous system neurons, behave as dependence receptors: they instruct neurons to die if there is no ligand around. By contrast, TrkB, expressed mainly in the central nervous system, does not signal death in the absence of ligand.
- Vassiliki Nikoletopoulou
- , Heiko Lickert
- & Yves-Alain Barde
-
Letter |
The PtdIns(3,4)P2 phosphatase INPP4A is a suppressor of excitotoxic neuronal death
The enzyme inositol polyphosphate phosphatase 4A (INPP4A) removes phosphate groups from phosphatidylinositol-3,4-bisphosphate, a key cellular lipid. Here, a crucial role for INPP4A in maintaining the integrity of the brain is described. Mice that lack this enzyme suffer from neurodegeneration in the striatum of the brain, as well as severe involuntary movements. When present, INPP4A protects neurons from a particular type of cell death.
- Junko Sasaki
- , Satoshi Kofuji
- & Takehiko Sasaki
Neuronal diversity and convergence in a visual system developmental atlas