Brain and brawn: parallels in oxidative strength

Topic: Brain proteins, microglia and lab models

Neuronal oxidative stress occurs early in the progression of Alzheimer disease (AD), significantly before the development of the pathologic hallmarks, neurofibrillary tangles, and senile plaques. Study of Down syndrome, cases with autosomal dominant mutation, and sporadic AD all suggest amyloid-beta deposition and hyperphosphorylated tau function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative damage. Amyloid-beta and tau hyperphosphorylation also define vulnerable muscle cells in sporadic inclusion-body myositis (s-IBM). The role of the structural changes of s-IBM, as in AD, remains to be determined but may mark a critical response yielding a novel balance in oxidant homeostasis.

@article{moreira2006-16432155,
  author  = {Moreira, P. I. and Honda, K. and Zhu, X. and Nunomura, A. and Casadesus, G. and Smith, M. A. and Perry, G.},
  title   = {{Brain and brawn: parallels in oxidative strength}},
  journal = {Neurology},
  year    = {2006},
  doi     = {10.1212/01.wnl.0000192307.15103.83},
  pmid    = {16432155},
  url     = {https://doi.org/10.1212/01.wnl.0000192307.15103.83}
}

Key findings

• Neuronal oxidative stress occurs early in the progression of Alzheimer disease (AD), significantly before the development of the pathologic hallmarks, neurofibrillary tangles, and senile plaques.

Why it matters

This review proposes that oxidative stress occurs early in Alzheimer disease and that amyloid-beta and tau changes may be compensatory responses. It discusses a similar process in a muscle disease, but it does not report a treatment or cure.

Study details

• Evidence strengthLow

Read the original

• DOI: 10.1212/01.wnl.0000192307.15103.83
• PubMed: 16432155
• Original source →

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Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here.

• Neuropathology of human Alzheimer disease after immunization with amyloid-beta peptide: a case report Nature medicine · 2003-03-17 · usefulness score 61/100 · Brain tissue and pathology
• Oxidative damage is the earliest event in Alzheimer disease Journal of neuropathology and experimental neurology · 2001-08-01 · usefulness score 52/100 · Genetics

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• Association between frontal cortex oxidative damage and beta-amyloid as a function of age in Down syndrome Biochimica et biophysica acta · 2011-10-08 · usefulness score 47/100
• Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia Current gerontology and geriatrics research · 2011-11-29 · usefulness score 46/100
• Restoration of aberrant mTOR signaling by intranasal rapamycin reduces oxidative damage: Focus on HNE-modified proteins in a mouse model of down syndrome Redox biology · 2019-03-09 · usefulness score 45/100
• The DSCR1 (Adapt78) isoform 1 protein calcipressin 1 inhibits calcineurin and protects against acute calcium-mediated stress damage, including transient oxidative stress FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2002-06-01 · usefulness score 42/100

Also tagged “down”

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• State-of-the-art therapy for Down syndrome Developmental medicine and child neurology · 2023-01-24 · usefulness score 42/100 · Down syndrome and Alzheimer's
• Cytonectin expression in Alzheimer disease Journal of neuropathology and experimental neurology · 2002-03-01 · usefulness score 27/100 · Down syndrome and Alzheimer's
• Growth properties and in vitro life span of Alzheimer disease and Down syndrome fibroblasts. A blind study Mechanisms of ageing and development · 1990-03-01 · usefulness score 30/100 · Down syndrome and Alzheimer's

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More on Down syndrome and Alzheimer's

• A review that covers this ground Oxidative stress and mitochondrial dysfunction in Down syndrome Advances in experimental medicine and biology · 2012-01-01 · usefulness score 41/100
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