Literature DB >> 8512210

The lysosomal system in neuronal cell death: a review.

R A Nixon1, A M Cataldo.   

Abstract

The lysosomal system has often been considered a prominent morphologic marker of distressed or dying neurons. Lysosomes or their constituent hydrolases have been viewed in different neuropathologic states as either initiators and direct agents of cell death, agents of cellular repair and recompensation, effectors of end-stage cellular dissolution, or autolytic scavengers of cellular debris. Limited data and limitations of methodology often do not allow these potential roles to be discriminated. In all forms of neurodegeneration, it may be presumed that lysosomes ultimately rupture and release various hydrolases that promote cell autolysis during the final stages of cellular disintegration. Beyond this perhaps universal contribution to cell death, the degree to which the lysosomal system may be involved in neurodegenerative states varies considerably. In many conditions, morphologic evidence for activation of the lysosomal system is minimal or undetectable. In other cases, lysosomal activation is evident only when other morphologic signs of cell injury are also present. This level of participation may be viewed as either an attempt by the neuron to compensate for or repair the injury or a late-stage event leading to cell dissolution. The early involvement of the lysosomal system in neurodegeneration occurs most commonly in the form of intraneuronal accumulations of abnormal storage profiles or residual bodies (tertiary lysosomes). Very often the lysosomal involvement can be traced to a primary defect or dysfunction of lysosomal components or to accelerated or abnormal membrane breakdown that leads to the buildup of modified digestion-resistant substrates within lysosomes. Because they are often striking, changes in the lysosomal system are a sensitive morphologic indicator of certain types of metabolic distress; however, whether they reflect a salutary response of a compromised neuron or a mechanism to promote cell death and removal of debris from the brain remains to be established for most conditions. Factors that may influence the lysosomal response during lethal neuronal injury include species differences, stage of neuronal development, duration of injury and pace of cell death. The lysosomal system may be more closely coupled to certain forms of neuronal cell death in lower vertebrate or invertebrate systems than in mammalian systems.

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Year:  1993        PMID: 8512210     DOI: 10.1111/j.1749-6632.1993.tb18291.x

Source DB:  PubMed          Journal:  Ann N Y Acad Sci        ISSN: 0077-8923            Impact factor:   5.691


  19 in total

Review 1.  The endosomal-lysosomal system of neurons in Alzheimer's disease pathogenesis: a review.

Authors:  R A Nixon; A M Cataldo; P M Mathews
Journal:  Neurochem Res       Date:  2000-10       Impact factor: 3.996

2.  ATM is a cytoplasmic protein in mouse brain required to prevent lysosomal accumulation.

Authors:  C Barlow; C Ribaut-Barassin; T A Zwingman; A J Pope; K D Brown; J W Owens; D Larson; E A Harrington; A M Haeberle; J Mariani; M Eckhaus; K Herrup; Y Bailly; A Wynshaw-Boris
Journal:  Proc Natl Acad Sci U S A       Date:  2000-01-18       Impact factor: 11.205

3.  Targeted delivery of proteins across the blood-brain barrier.

Authors:  Brian J Spencer; Inder M Verma
Journal:  Proc Natl Acad Sci U S A       Date:  2007-04-26       Impact factor: 11.205

4.  Increased neuronal endocytosis and protease delivery to early endosomes in sporadic Alzheimer's disease: neuropathologic evidence for a mechanism of increased beta-amyloidogenesis.

Authors:  A M Cataldo; J L Barnett; C Pieroni; R A Nixon
Journal:  J Neurosci       Date:  1997-08-15       Impact factor: 6.167

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

Authors:  Ying Jiang; Yutaka Sato; Eunju Im; Martin Berg; Matteo Bordi; Sandipkumar Darji; Asok Kumar; Panaiyur S Mohan; Urmi Bandyopadhyay; Antonio Diaz; Ana Maria Cuervo; Ralph A Nixon
Journal:  J Neurosci       Date:  2019-05-01       Impact factor: 6.167

6.  Resistance to tumor necrosis factor-induced cell death mediated by PMCA4 deficiency.

Authors:  K Ono; X Wang; J Han
Journal:  Mol Cell Biol       Date:  2001-12       Impact factor: 4.272

7.  Hepatic disposal of advanced glycation end products during maturation and aging.

Authors:  Dmitri Svistounov; Ana Oteiza; Svetlana N Zykova; Karen Kristine Sørensen; Peter McCourt; Andrew J McLachlan; Robert S McCuskey; Bård Smedsrød
Journal:  Exp Gerontol       Date:  2013-03-24       Impact factor: 4.032

Review 8.  Cysteine cathepsins in neurological disorders.

Authors:  Anja Pišlar; Janko Kos
Journal:  Mol Neurobiol       Date:  2013-11-15       Impact factor: 5.590

9.  Lysosomal activity associated with developmental axon pruning.

Authors:  Jae W Song; Thomas Misgeld; Hyuno Kang; Sharm Knecht; Ju Lu; Yi Cao; Susan L Cotman; Derron L Bishop; Jeff W Lichtman
Journal:  J Neurosci       Date:  2008-09-03       Impact factor: 6.167

10.  Identification of S-sulfonation and S-thiolation of a novel transthyretin Phe33Cys variant from a patient diagnosed with familial transthyretin amyloidosis.

Authors:  Amareth Lim; Tatiana Prokaeva; Mark E McComb; Lawreen H Connors; Martha Skinner; Catherine E Costello
Journal:  Protein Sci       Date:  2003-08       Impact factor: 6.725

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