Neurology -- Correspondence for Launer et al., 57 (8) 1447-1452

Correspondence published:

High density lipoproteins as hidden imprint of Alzheimer's brain cholesterol pathology: Alexei R Koudinov, "Temirbolat T Berezov, Natalia V Koudinova" (12 December 2001)

High density lipoproteins as hidden imprint of Alzheimer's brain cholesterol pathology 12 December 2001

Alexei R Koudinov,
neuroscientists
Russian Acad Med Sciences, Moscow, Russia; Weizmann Inst., Dept. Biol. Regulation, Rehovot, Israel,
"Temirbolat T Berezov, Natalia V Koudinova"
Send Correspondence to journal:
Re: High density lipoproteins as hidden imprint of Alzheimer's brain cholesterol pathology

koudin{at}imb.ac.ru Alexei R Koudinov, et al.

To the editor:
We read with great interest recent Neurology contribution by Launer et al. [ 1 ] and thank the authors for their excellent work.
We recently investigated different aspects of cholesterol involvement in Alzheimer’s pathology. We reported on the essential role for cholesterol in synaptic function, plasticity and neuronal degeneration [ 2 ].
We also showed that Alzheimer’s CSF is characterized by increased soluble amyloid b (Ab) and apolipoprotein content of the high density lipoprotein 1 (HDL₁), that are negligible in controls.[ 3 ]
In the central nervous system, HDL₁ was proposed to mediate a role in cholesterol redistribution and reverse cholesterol transport by analogy with enriched in cholesterol plasma HDL.[ 3 ]
Launer's observation et al. [ 1 ] of the correlation of Alzheimer’s histochemical features with systemic HDL cholesterol in association with our data [ 3 ] and another earlier article by Merched et al. [ 4 ] further strengthens Launer's conclusion that “the constituents of HDL cholesterol may play a role in the formation of AD pathology, and these processes are reflected in peripheral measures”.
These data also [ 1, 3, 4 ] support our proposed hypothesis that upregulation of brain cholesterol dynamics (requiring higher demands for reverse transport of cholesterol by HDL [ 3 ]) is a key phenomenon in sporadic AD.
On the other hand, the strong linear association between increasing late-life HDL cholesterol levels and an increasing number of neocortical neuritic plaques and hippocampal and neocortical neurofibrillary tangles [ 1 ] in our view supports our proposed idea that tau and Ab neurochemistry change are secondary phenomena aiming to compensate impaired cholesterol homeostasis or associated synaptic plasticity and neurotransmission impairment, or both. ( 2 and 5 ).
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References:
1. Launer LJ, White LR, Petrovitch H, Ross GW, Curb JD. Cholesterol and neuropathologic markers of AD: A population-based autopsy study. Neurology 2001; 57: 1447-1452 [ PubMed ] [ Full Text ].
2. Koudinov AR, Koudinova NV. Essential role for cholesterol in synaptic plasticity and neuronal degeneration. FASEB J. 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 ].
3. Koudinov AR, Berezov TT, Koudinova NV. The levels of soluble amyloid beta in different high density lipoprotein subfractions distinguish Alzheimer’s and normal aging CSF: implication for brain cholesterol pathology? Neurosci. Lett. 2001; 314: 115-118 [ Full Text ] [ PubMed ] [ Reprint Order ].
4. Merched A, Xia Y, Visvikis S, Serot JM, Siest G. Decreased high-density lipoprotein cholesterol and serum apolipoprotein AI concentrations are highly correlated with the severity of Alzheimer's disease.
Neurobiol Aging. 2000; 21: 27-30 [ PubMed ].
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 ].

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