PAPER Catalá-López F, Crespo-Facorro B, Vieta E, Valderas JM, Valencia A, Tabarés-Seisdedos R
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PAPER Abner EL, Nelson PT, Schmitt FA, Browning SR, Fardo DW, Wan L, Jicha GA, Cooper GE, Smith CD, Caban-Holt AM, Van Eldik LJ, Kryscio RJ
Self-Reported Head Injury and Risk of Late-Life Impairment and AD Pathology in an AD Center Cohort.
Dement Geriatr Cogn Disord. 2014;37(5-6):294-306. Epub 2013 Dec 31 PubMed: 24401791PAPER Cutuli D, De Bartolo P, Caporali P, Tartaglione AM, Oddi D, D'Amato FR, Nobili A, D'Amelio M, Petrosini L
Neuroprotective effects of donepezil against cholinergic depletion.
Alzheimers Res Ther. 2013 Oct 24;5(5):50. PubMed: 24401551PAPER Windisch M
We can treat Alzheimer's disease successfully in mice but not in men: failure in translation? A perspective.
Neurodegener Dis. 2014;13(2-3):147-50. Epub 2014 Jan 7 PubMed: 24401335PAPER Van Dijk D
Long-term cognitive impairment after critical illness.
N Engl J Med. 2014 Jan 9;370(2):185. PubMed: 24401071PAPER Fraser GL, Riker RR, Coursin DC
Long-term cognitive impairment after critical illness.
N Engl J Med. 2014 Jan 9;370(2):184. PubMed: 24401070PAPER Pandharipande PP, Girard TD, Ely EW
Long-term cognitive impairment after critical illness.
N Engl J Med. 2014 Jan 9;370(2):185-6. PubMed: 24401069Michael Siciliano
Arlington, United States
Douglas Galasko on Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial.
COMMENT The TEAM-AD study revives interest in two areas: treatment with antioxidants such as vitamin E, and carrying out clinical trials in patients with mild to moderate AD to evaluate effects on disease progression. The findings of a benefit in the vitamin E tr
Benjamin Wolozin on Therapeutic modulation of eIF2α phosphorylation rescues TDP-43 toxicity in amyotrophic lateral sclerosis disease models.
COMMENT This is a great article. The approach makes classic use of genetics to identify TDP-43 interactors, and in the process identifies a number of previously known and unknown players. The most interesting parts of the article for me are the experiments modula
Kurt A. Jellinger on Head trauma and in vivo measures of amyloid and neurodegeneration in a population-based study.
COMMENT Mielke et al. found that among older people with MCI but not cognitively normal (CN) individuals, those with a previous history of traumatic brain injury (TBI) have more Aß deposits in the brain than those without TBI history, suggesting that the etiology
PAPER Roberts GW, Gentleman SM, Lynch A, Graham DI
beta A4 amyloid protein deposition in brain after head trauma.
Lancet. 1991 Dec 7;338(8780):1422-3. PubMed: 1683421PAPER Rudelli R, Strom JO, Welch PT, Ambler MW
Posttraumatic premature Alzheimer's disease. Neuropathologic findings and pathogenetic considerations.
Arch Neurol. 1982 Sep;39(9):570-5. PubMed: 7115146PAPER Mathis CA, Kuller LH, Klunk WE, Snitz BE, Price JC, Weissfeld LA, Rosario BL, Lopresti BJ, Saxton JA, Aizenstein HJ, McDade EM, Kamboh MI, DeKosky ST, Lopez OL
In vivo assessment of amyloid-β deposition in nondemented very elderly subjects.
Ann Neurol. 2013 Jun;73(6):751-61. Epub 2013 Apr 17 PubMed: 23596051Sam Gandy on Head trauma and in vivo measures of amyloid and neurodegeneration in a population-based study.
COMMENT I think that there a lot of uncontrolled and unknowable variables at work here. The post traumatic brain injury (TBI) amyloidosis probably peaks very early and then might be resolved completely. I assume that the propensities for depositing and the speed
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