Berg MJ - Search Results

1

Faulty autolysosome acidification in Alzheimer's disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques.

Lee JH, Yang DS, Goulbourne CN, Im E, Stavrides P, Pensalfini A, Chan H, Bouchet-Marquis C, Bleiwas C, Berg MJ, Huo C, Peddy J, Pawlik M, Levy E, Rao M, Staufenbiel M, Nixon RA. Lee JH, et al. Among authors: berg mj. Nat Neurosci. 2022 Jun;25(6):688-701. doi: 10.1038/s41593-022-01084-8. Epub 2022 Jun 2. Nat Neurosci. 2022. PMID: 35654956 Free PMC article.

2

Endosomal Dysfunction Induced by Directly Overactivating Rab5 Recapitulates Prodromal and Neurodegenerative Features of Alzheimer's Disease.

Pensalfini A, Kim S, Subbanna S, Bleiwas C, Goulbourne CN, Stavrides PH, Jiang Y, Lee JH, Darji S, Pawlik M, Huo C, Peddy J, Berg MJ, Smiley JF, Basavarajappa BS, Nixon RA. Pensalfini A, et al. Among authors: berg mj. Cell Rep. 2020 Nov 24;33(8):108420. doi: 10.1016/j.celrep.2020.108420. Cell Rep. 2020. PMID: 33238112 Free PMC article.

3

Lysosomal Dysfunction in Down Syndrome Is APP-Dependent and Mediated by APP-βCTF (C99).

Jiang Y, Sato Y, Im E, Berg M, Bordi M, Darji S, Kumar A, Mohan PS, Bandyopadhyay U, Diaz A, Cuervo AM, Nixon RA. Jiang Y, et al. J Neurosci. 2019 Jul 3;39(27):5255-5268. doi: 10.1523/JNEUROSCI.0578-19.2019. Epub 2019 May 1. J Neurosci. 2019. PMID: 31043483 Free PMC article.

4

Axonal transport of late endosomes and amphisomes is selectively modulated by local Ca²⁺ efflux and disrupted by PSEN1 loss of function.

Lie PPY, Yoo L, Goulbourne CN, Berg MJ, Stavrides P, Huo C, Lee JH, Nixon RA. Lie PPY, et al. Among authors: berg mj. Sci Adv. 2022 Apr 29;8(17):eabj5716. doi: 10.1126/sciadv.abj5716. Epub 2022 Apr 29. Sci Adv. 2022. PMID: 35486730 Free PMC article.

5

Autophagy flux in CA1 neurons of Alzheimer hippocampus: Increased induction overburdens failing lysosomes to propel neuritic dystrophy.

Bordi M, Berg MJ, Mohan PS, Peterhoff CM, Alldred MJ, Che S, Ginsberg SD, Nixon RA. Bordi M, et al. Among authors: berg mj. Autophagy. 2016 Dec;12(12):2467-2483. doi: 10.1080/15548627.2016.1239003. Epub 2016 Nov 4. Autophagy. 2016. PMID: 27813694 Free PMC article.

6

Single-walled carbon nanotubes alleviate autophagic/lysosomal defects in primary glia from a mouse model of Alzheimer's disease.

Xue X, Wang LR, Sato Y, Jiang Y, Berg M, Yang DS, Nixon RA, Liang XJ. Xue X, et al. Nano Lett. 2014 Sep 10;14(9):5110-7. doi: 10.1021/nl501839q. Epub 2014 Aug 21. Nano Lett. 2014. PMID: 25115676 Free PMC article.

7

Neurofilament light interaction with GluN1 modulates neurotransmission and schizophrenia-associated behaviors.

Yuan A, Veeranna, Sershen H, Basavarajappa BS, Smiley JF, Hashim A, Bleiwas C, Berg M, Guifoyle DN, Subbanna S, Darji S, Kumar A, Rao MV, Wilson DA, Julien JP, Javitt DC, Nixon RA. Yuan A, et al. Transl Psychiatry. 2018 Aug 24;8(1):167. doi: 10.1038/s41398-018-0194-7. Transl Psychiatry. 2018. PMID: 30143609 Free PMC article.

8

mTOR hyperactivation in Down Syndrome underlies deficits in autophagy induction, autophagosome formation, and mitophagy.

Bordi M, Darji S, Sato Y, Mellén M, Berg MJ, Kumar A, Jiang Y, Nixon RA. Bordi M, et al. Among authors: berg mj. Cell Death Dis. 2019 Jul 22;10(8):563. doi: 10.1038/s41419-019-1752-5. Cell Death Dis. 2019. PMID: 31332166 Free PMC article.

9

Functions of neurofilaments in synapses.

Yuan A, Sershen H, Veeranna, Basavarajappa BS, Kumar A, Hashim A, Berg M, Lee JH, Sato Y, Rao MV, Mohan PS, Dyakin V, Julien JP, Lee VM, Nixon RA. Yuan A, et al. Mol Psychiatry. 2015 Aug;20(8):915. doi: 10.1038/mp.2015.99. Mol Psychiatry. 2015. PMID: 26201270 Free PMC article. No abstract available.

10

Neurofilament subunits are integral components of synapses and modulate neurotransmission and behavior in vivo.

Yuan A, Sershen H, Veeranna, Basavarajappa BS, Kumar A, Hashim A, Berg M, Lee JH, Sato Y, Rao MV, Mohan PS, Dyakin V, Julien JP, Lee VM, Nixon RA. Yuan A, et al. Mol Psychiatry. 2015 Aug;20(8):986-94. doi: 10.1038/mp.2015.45. Epub 2015 Apr 14. Mol Psychiatry. 2015. PMID: 25869803 Free PMC article.

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