PT  - JOURNAL ARTICLE
AU  - Squitti, R.
AU  - Barbati, G.
AU  - Rossi, L.
AU  - Ventriglia, M.
AU  - Dal Forno, G.
AU  - Cesaretti, S.
AU  - Moffa, F.
AU  - Caridi, I.
AU  - Cassetta, E.
AU  - Pasqualetti, P.
AU  - Calabrese, L.
AU  - Lupoi, D.
AU  - Rossini, P. M.
TI  - Excess of nonceruloplasmin serum copper in AD correlates with MMSE, CSF β-amyloid, and h-tau
AID  - 10.1212/01.wnl.0000223343.82809.cf
DP  - 2006 Jul 11
TA  - Neurology
PG  - 76--82
VI  - 67
IP  - 1
4099  - http://n.neurology.org/content/67/1/76.short
4100  - http://n.neurology.org/content/67/1/76.full
SO  - Neurology2006 Jul 11; 67
AB  - Objective: To assess whether serum copper in Alzheimer disease (AD) correlates with cognitive scores, β-amyloid, and other CSF markers of neurodegeneration. Methods: The authors studied copper, ceruloplasmin, total peroxide, and antioxidants levels (TRAP) in serum; β-amyloid in plasma; and copper, β-amyloid, h-tau, and P-tau in the CSF of 28 patients with AD and 25 healthy controls, in relation to clinical status. Results: Serum copper (p < 0.0001), peroxides (p = 0.002), a copper fraction unexplained by ceruloplasmin (p < 0.0001), and CSF h-tau (p = 0.001) were increased in AD, whereas serum TRAP (p = 0.03) and CSF β-amyloid were decreased (p < 0.0001). Plasma β-amyloid increased with age in healthy controls (r = 0.6; p = 0.05). CSF markers of AD correlated with serum copper variables. CSF copper was partially dependent on the serum copper fraction unexplained by ceruloplasmin (t = 2.2, p = 0.04). CSF β-amyloid seemed to be related to serum copper (r = −0.46; p = 0.002). Mini-Mental Status Examination scores correlated positively with β-amyloid (r = 0.46, p = 0.002) and inversely with copper unexplained by ceruloplasmin (r = −0.45, p = 0.003). Conclusions: The authors' results confirm the existence of changes in copper component distribution, particularly the copper fraction unexplained by ceruloplasmin and support the hypothesis of a β-amyloid and copper connection in Alzheimer disease.