Review Reports

Round 1

Reviewer 1 Report

Comments and Suggestions for Authors

The authors describe a case report of a patient with Posterior Cortical Athrophy a rather common (5-15%) presentation of Alzheimer's disease who was treated for tick-borne illness (Bartonella) , mycotoxins and heavy metals along with a plant rich ketogenic diet and vision excercises and training among others. The treatment led to not only slowing decline but improvement of her symptoms and MRI volumetrics.

They present their results with adequate data and Figures and they analyze their results appropriately.

Since the slowing and more importantly improvement of the symptoms of Alzheimer's disease and its relevant presentations such as PCA is of great interest to the scientific community, I believe that the submitted case report adds to the common knowledge about PCA and points to a more personalized treatment of patients after additional lab testing and evaluation. Environmental factors seem to have an increasingly important role and should be included in the lab testing of patients.

Results are adequately described, Tables and Figures support the results and are valuable to the reader understanding. Discussion and Conclusions are supported by the results. Minor syntax and typographical errors could be assessed during proofreading.

English is fine and minor errors could be corrested during proofreading.

Author Response

Please see the attachment.

Author Response File: Author Response.pdf

Reviewer 2 Report

Comments and Suggestions for Authors

1. The novelty would benefit from a more precise comparison to existing literature on infectious etiologies in Alzheimer’s disease (AD) variants. For instance, while the contagious theory of AD is cited, the direct linkage to PCA-specific outcomes (e.g., MRI volumetrics improvement) needs deeper contextualization with prior studies (e.g., Bredesen’s 2016 work on inhalational AD).

 

2. The hypothesis that treating Bartonella and mycotoxins reverses PCA symptoms is intriguing but requires more vigorous mechanistic justification. The discussion briefly mentions TGF-β1 and p-tau181 but does not elaborate on how these biomarkers mechanistically connect to the observed clinical improvements. A more detailed pathway analysis—such as how Bartonella infection might exacerbate tau pathology or neuroinflammation—would strengthen the theoretical framework. Additionally, the role of EWOT (Exercise with Oxygen Therapy) in symptom improvement is noted anecdotally; a physiological rationale (e.g., enhanced cerebral oxygenation or mitochondrial function) should be included.

 

3. While the case study is well-documented, the absence of a control or comparator group limits the generalizability of the findings. The authors should address how confounding variables (e.g., concurrent supplements, dietary changes) were controlled. Furthermore, the timeline of interventions (e.g., 3 months for Bartonella vs. 2.5 years for mycotoxins) lacks justification. A table summarizing treatment phases with hypothesized targets (e.g., infection clearance vs. detoxification) would improve clarity.

 

4. The results demonstrate impressive improvements in MRI volumetrics and cognitive function, but the discussion oversimplifies causality.

 

5. Minor Notes, for example, Typo: "simultanagnosis" → "simultanagnosia" (Page 3); Abbreviations (e.g., EWOT) should be defined at first use.

Author Response

Please see the attachment.

Author Response File: Author Response.pdf