Neurology -- Correspondence for Jaworska-Wilczynska et al., 58 (3) 438-445

Correspondence published:

Cholesterol disbalance at neuromuscular junctions and CNS synapses: a unifying cause of degeneration: Alexei Koudinov, Natalia Koudinova and Ulrike Beisiegel (26 February 2002)

Cholesterol disbalance at neuromuscular junctions and CNS synapses: a unifying cause of degeneration 26 February 2002

Alexei Koudinov,
neuroscientist
Medizinische Klinik, U. Eppendorf, Hamburg, Germany; Berezov Acad Lab, Acad Med Sci, Moscow, Russia,
Natalia Koudinova and Ulrike Beisiegel
Send Correspondence to journal:
Re: Cholesterol disbalance at neuromuscular junctions and CNS synapses: a unifying cause of degeneration

koudinov{at}usa.net Alexei Koudinov, et al.

We appreciate timely contribution by Jaworska-Wilczynska et al. that appeared in February 12, 2002 Neurology issue [ 1 ]. This important article supports previous reports on the physiological role for lipoprotein receptors in transsynaptic signaling pathways [ 2 ] and discusses the role of cholesterol in amyloid protein precursor processing and amyloid buildup [ 1 ].
The discussion does not cover the role of cholesterol in the normal function, plasticity and pathologic failure of CNS synapses [ 3 ] and neuromuscular junction [ 4 ]. This would not only help to unite the pathophysiological basis and secondary features (that is amyloid and tau pathology) of inclusion-body myositis [ 1 ] and Alzheimer's neurodegeneration [ 5 ], but would also reiterate the neurodegeneration in PD and ALS (characterized by tau abnormality and unique neuroanatomical/neurotransmitter system and oxidative stress pathway dysfunction, respectively, also [ 6 ]) opening the discussion for disease specificity of neurodegeneration.

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References:
1. Jaworska-Wilczynska M, Wilczynski GM, Engel WK, Strickland DK, Weisgraber KH, Askanas V. Three lipoprotein receptors and cholesterol in inclusion-body myositis muscle. Neurology. 58, 438-445 (2001) [ PubMed ] [ Full Text ].
2. Koudinov AR, Koudinova NV. LRP: a cholesterol recruitment checkpoint for neuronal structure-functional plasticity? J Clin Invest. published online 12 October 2001 [ Full Text ]; Zhuo M, Holtzman DM, Li Y, et al. Role of tissue plasminogen activator receptor LRP in hippocampal long-term potentiation. J Neurosci. 20, 542-549 (2000) [ PubMed ].
3. Koudinov AR, Koudinova NV. Essential role for cholesterol in synaptic plasticity and neuronal degeneration. FASEB J. 15, 1858-1860 (2001), originally published online June 27, 2001, 10.1096/fj.00-0815fje [ Article Preface at the authors WEB site ] [ Abstract and Full text at FASEB J ] [ PubMed ] [ Authors related eLetters to editor ];
4. Naguib M, Flood P, McArdle JJ, Brenner HR. Advances in neurobiology of the neuromuscular junction: implications for the anesthesiologist. Anesthesiology. 96, 202-231 (2002) [ PubMed ] [ Full text ].
5. Koudinov AR, Koudinova NV. Brain Cholesterol Pathology is the Cause of Alzheimer's Disease. Clin. Med. Health Res. published online November 27, 2001, clinmed/2001100005 [ Article Preface at the authors WEB site ] [ Abstract and Full text at Clin Med J ] [ Authors related eLetters to editor ]; Koudinov AR, Berezov TT, Koudinova NV. Cholesterol and Alzheimer's disease: Is there a link? Neurology (2002) In press [ Neurology online edition ].
6. Spillantini MG, Goedert M. Tau and Parkinson disease. JAMA. 286, 2324-2326 (2001) [ PubMed ] [ Full text ]; Shefner JM, Brown RH Jr, Cole D, et al. Effect of neurophilin ligands on motor units in mice with SOD1 ALS mutations. Neurology. 57, 1857-1861 (2001) [ PubMed ]; Mase G, Ros S, Gemma A, et al. ALS with variable phenotypes in a six-generation family caused by leu144phe mutation in the SOD1 gene. J Neurol Sci. 191, 11-18 (2001) [ PubMed ].

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