Alzheimer’s Disease & Peptide Research

Cross-sectional LC–MS/MS plasma measurements. Table 1 and Figure 1 report group distributions and ROC analysis.

• The assay needs independent validation against other causes of cognitive impairment. The authors disclose related patent interests. The study did not administer HAEE.

Selected methods and findings in the original article.

The authors measured brain homogenates three days after intracerebroventricular oligomeric amyloid-β injection and a course of HAEE. Figure 1 lists n=8 for the brain measurements.

• This acute experimental challenge and the cell assays address clearance mechanisms. Clinical effects remain unknown.

Selected methods and findings in the original article.

The investigators combined molecular binding assays with a transgenic nematode model to test the interaction between zinc, isomerized amyloid-β and HAEE.

• The findings apply to molecular and nematode experiments.

Selected methods and findings in the original article.

The abstract reports intravenous radiotracer experiments in mice, amyloid binding by calorimetry and experiments in cells and nematodes.

• The numerical estimates come from the conference abstract. The companion journal abstract describes its radiolabeled half-life comparison as approximately twofold. Human pharmacokinetics remain uncharacterized.

Original abstract.

Iodine-125 radiotracer measurements, isothermal titration calorimetry, western blotting, ELISA and flow cytometry.

• The journal abstract omits detailed group estimates. The conference abstract is a companion report from the same research program.

Original abstract.

50 participants per group at enrollment. The treatment group received 20 intravenous infusions of 20 mL in 100 mL saline over four weeks, annually for three years. The comparison group received no placebo infusions. The analysis included 48 treated and 46 comparison participants.

• Open comparison without placebo infusions. The authors describe random allocation with limited procedural detail.
• Six participants were absent from the completer analysis. The study does not establish dementia prevention.
• This was an open study with a completer analysis. A placebo-controlled replication with masked assessment would clarify the dementia-conversion result.

Original Russian article, Tables 3–4.

Double-blind trial. 76 assigned to Cerebrolysin and 73 to placebo. Intravenous 30 mL five days weekly for four weeks, repeated after a two-month treatment-free interval.

• The trial followed patients for 28 weeks and does not establish a lasting effect on disease progression.

Original abstract.

Randomized double-blind groups received 10 mL (69), 30 mL (70), 60 mL (71) or placebo (69). Infusions were given five days weekly for four weeks, then twice weekly for eight weeks.

• Cognitive findings varied by dose. The abstract omits detailed score differences and adverse-event counts.

Original abstract.

Pooled estimates of cognition and global clinical change from randomized placebo-controlled trials.

• The pooled data include previously reported trials. The six-month cognitive estimate was inconclusive.

Original abstract.

Semax or Met-Glu-Asp-Arg-Pro-Gly-Pro at 50 μg/kg intranasally every other day for 15 doses. Controls were untreated APP/PS1 and wild-type mice. Histology figures report n=10 per group.

• An animal Alzheimer’s model does not establish clinical efficacy or safety in people.
• The derivative and Semax are distinct preparations; results must not be treated as interchangeable.
• The derivative includes EDR within a different molecule. The study did not test standalone Pinealon.

Full article, Figures 6–7.

Uncontrolled before-and-after observations in 25 patients: 13 with mild and 12 with moderate dementia. The disclosure describes 18–20 mg/day of intranasal Semax and reports the same group across examples.

• The patent provides no concurrent placebo group. Changes cannot be separated from other influences, and the report does not establish treatment benefit.
• Patents record claimed inventions and supporting disclosures. Publication or grant does not establish clinical efficacy, safety or marketing approval. Members of one patent family and related journal reports can describe the same experiments.
• Status labels are Google Patents index snapshots for the displayed publication or application; each record lists the review date. Official registers and every national family member have not been independently checked. These labels do not establish freedom to operate.

Original patent text, selected examples and tables.

Separate electrophysiology and spine-morphology experiments; each lists four groups of ten mice, five of each sex. Slices/cells are nested observations, not extra animals.

• Mouse findings do not establish human cognitive or Alzheimer’s treatment benefit.
• Confirm statistical handling of nested slice/cell measurements and inconsistent spine-subtype values.
• Effects differ by sex and spine subtype. Check the statistical treatment of nested observations and inconsistent subtype values before further extraction. This is not a clinical Alzheimer’s trial.

Original full-text XML; methods and results narrative, not graph digitization

Noopept 0.01 mg/kg for 21 days plus five training days. Spatial memory was assessed with the Morris water maze and serum antibodies with ELISA.

• The abstract omits group sizes and a numerical behavioral effect size. The serum response does not quantify plaque clearance.

Original abstract.

Differentiated PC12 cells received 10 μM Noopept for 72 hours before exposure to 5 μM amyloid-β(25–35). The tau assay used four independent experiments with three replicate wells.

• An acute cell assay cannot establish effects on clinical tau pathology or cognition.

Selected methods and findings in the original article.