Skip to main content
. 2022 Jul 19;23(14):7935. doi: 10.3390/ijms23147935

Table 2.

Possible links between Alzheimer’s Disease (AD) and Mo deficiency or/and Cu–Mo–S altered metabolism.

Event Research Results
NCp–Cu accumulation in serum or
plasma.

  1. Chronic exposure to Cu and its dyshomeostasis has been linked to accelerated cognitive decline and potentially increased the risk of AD [41,42,43];

  2. High nCp–Cu in the serum characterizes AD patients [36];

  3. Serum Cu was inversely associated with testosterone [23] and Rosario et al. [22] found that brain levels of testosterone are significantly lower in AD.
Cu and Mo are antagonists, so excessive
Cu cause Mo deficiency and vice versa.

  1. The formation of a Cu–Mo complex can be the place of nutritional interaction between the two metal ions [116];

  2. Cu–Mo complex was unavailable for ceruloplasmin synthesis [117];

  3. Excess in Cu supply and a non-absorbable complex of Cu and Mo in the gastrointestinal tract might reduce Mo absorption [114];

  4. Reducing uptake or retention of Mo in Cu-deficient induces Cu-excess in rats [114];

  5. Increased cellular Cu contents might be causal for a decreased rate of Moco synthesis [97];

  6. Competition between Cu, at a high level, and Mo occurs during Moco formation [119];

  7. Cu/Mo ratio imbalance affects S metabolism [123].
Products of enzymes’ activity that have
Mo as a co-factor are in lower content
in AD than in healthy people

  1. A high Cu/Mo ratio affects xanthine oxidase activity [121];

  2. Decreased contents of adenosine, guanosine, hypoxanthine, and xanthine in early AD frontal cortex [86];

  3. High serum uric acid contents were significantly associated with decreased risk of AD, so patients with gout may have reduced risk for AD [86,89];

  4. AD patients/models demonstrate reductions in adenylyl cyclase activity [102,103].
Altered S amino acids metabolism
occurs in AD

  1. Mo is the sulfite oxidase (SUOX) co-factor: its low activity damages S metabolism [9,10];

  2. AD has a high Cys/SO42− ratio in plasma [7].;

  3. In AD, there is a plasma decrease of SO42− level [7] (low SO42− content indicates low SUOX activity due to possible Mo or Moco deficiency);

  4. Cys levels are high in AD plasma [7];

  5. Cys decreased by ca. 3-fold in the brain of a rat model of AD [57];

  6. Cytochrome c is the electron acceptor for the SUOX. COX activity from AD was decreased significantly in platelets and the hippocampus [95];

  7. High nCp–Cu causes an accumulation of Hcy due to a decrease in Cystathionine b-synthase activity [122].
Mo contents

  1. AD: serum Mo level increased progressively, passing from healthy subjects (HS) through subjective memory complaint, mild cognitive impairment up to AD [124];

  2. Diabetic (T2D) with severe complications: serum Mo contents increased [30];

  3. T2D with severe complications: lower urine Mo contents [30].