BAT Levels Timeline: History of Alzheimer’s Disease & the Rise of BATWatch

Understanding brain health and the origins of Alzheimer’s disease requires more than just today’s research. At BATWATCH™, we believe that innovation stands on the shoulders of every breakthrough that came before it. That’s why our science and clinical teams have gone all the way back to the earliest days of Alzheimer’s research, gathering every milestone, study, and hypothesis from the historical archives to the latest peer-reviewed literature.

We’ve systematically collected, digitized, and analyzed over a century of scientific progress: from Dr. Alois Alzheimer’s first case report in 1907, to the discoveries of beta-amyloid and tau in the 1980s, through the biomarker revolution and today’s advances in plasma-based early detection.

By training our advanced AI models on this vast historical and contemporary data set, we’re able to spot patterns, validate protocols, and push the boundaries of brain health science, turning a century of discovery into actionable, preventive care.

Every data point, every study, and every landmark you’ll see below feeds directly into the BATWATCH™ Evidence Matrix – the living intelligence engine behind our patient protocols.

Want the full backstory behind these breakthroughs? Read the complete history of Alzheimer’s disease and the rise of BATWatch.

Our timeline below isn’t just a chronology, it’s the foundation of the BATWatch™ Protocol.

Explore how over a century of discovery has shaped the fight to end Alzheimer’s disease, through science, biomarkers, and the dawn of next-generation brain health prevention.

November 3, 1906
Discovery of Alzheimer’s Disease
Dr. Alois Alzheimer presents and publishes the first case of “presenile dementia,” describing hallmark plaques and tangles in the brain.
Timeline illustrating the history of Alzheimer’s disease and the rise of BATWatch.
Figure 1. Alois Alzheimer. About 1909.
 
Hippius H, Neundörfer G. The discovery of Alzheimer's disease. Dialogues Clin Neurosci. 2003 Mar;5(1):101-8. doi: 10.31887/DCNS.2003.5.1/hhippius. PMID: 22034141; PMCID: PMC3181715.
 
July 15, 1910
Kraepelin coined the term
‘Alzheimer’s disease’
Kraepelin mentions Alheimer's disease in the eighth edition of his Handbook of Psychiatry, declaring it to be a specific clinical-pathological disease entity.

Figure 3. (Left to right) A. Alzheimer, E. Kraepelin, R. Gaupp, and F. Nissl. About 1906. © Archive for History of Psychiatry, Department of Psychiatry University of Munich. With permission.

Kraepelin E. Psychiatrie. 8th ed. Vol I: Allgemeine Psychiatrie; Vol II: Klinische Psychiatrie. Leipzig, Germany: Barth; 1909/1910 [Google Scholar]

April 2, 1984
Identified Amyloid as the core plaque protein
Purified and characterized beta-amyloid as the core component of amyloid plaques in AD brains, establishing the first biochemical basis for amyloid-based biomarker testing.

Figure 1. Dr. George G. Glenner 1984. © George G. Glenner Alzheimer's Family Centers, Inc

Glenner GG & Wong CW (1984): Purified and characterized beta-amyloid as the core component of amyloid plaques in AD brains. PubMed

Dec 26, 1995
Identified Tau as a diagnostic marker
Staging of alzheimer’s disease-related neurofibrillary changes. Showed that increased tau protein levels in CSF are a sensitive and specific biomarker for Alzheimer’s disease, making modern BAT Testing™ possible.

Figure 1. Dr. Kaj Blennow 2023. © Johan Wingborg, University of Gothenburg

Blennow, K., Wallin, A., et al. (1995): Staging of alzheimer's disease-related neurofibrillary changes. PubMed

2000-2005
Aβ42/40 biomarker established as
gold-standard for Alzheimer's Risk
This period marked the shift from just measuring total beta-amyloid (or Aβ42 alone) to recognizing that the Aβ42/40 ratio in CSF (and later in blood) was much more accurate and specific for distinguishing early brain changes and Alzheimer’s pathology.

Figure 1. Niels Andreasen MD 2004. © ResearchGate GmbH.

2006-2010
Rapamycin shown to reduce amyloid and tau
in aging brain models (animal studies).
Major studies reveal that rapamycin can activate the brain’s natural cleanup systems (autophagy), reducing beta-amyloid and tau buildup in aging models. This opens the door to new prevention strategies for brain health.

Figure 1. Patricia R. Spilman, M.A. 2014. © Regents of University of California

Spilman, P., et al. (2010): Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease. PubMed

2011-2015
BAT biomarker testing recognized in clinical
guidelines for early brain health monitoring
Major clinical guidelines formally adopt beta-amyloid and tau as core markers for preclinical brain changes, making biomarker-based prevention and early detection part of mainstream clinical care.

Figure 1. Dr. Reisa Sperling 2024. © Board of Regents of the University of Wisconsin

Sperling, R. A., Jack, C. R., Aisen, P. S., et al. (2011): Toward defining the preclinical stages of Alzheimer's disease: PubMed

2011-2015
Blood-based BAT marker testing becomes
accurate and accessible for routine brain
health monitoring
First ultra-sensitive blood assays for Aβ42/40 and phosphorylated tau are validated in clinical studies, enabling accurate, non-invasive tracking for BAT Levels and making brain health screening practical at scale.

Figure 1. Sebastian Palmqvist, MD, PhD 2024. © Tove Smeds | American Psychiatric Association

Palmqvist, S., Janelidze, S., Stomrud, E., et al. (2019):Performance of Fully Automated Plasma Assays as Screening Tests for Alzheimer Disease–Related β-Amyloid Status: JAMA

May 2024
BATWatch launches in Arizona, pioneering proactive brain health.
June 2023
Confirmed: BAT Levels can be lowered in humans.
BATWatch’s clinical team uncovers robust evidence that BAT Levels can be actively reduced in humans, marking a major shift from earlier animal studies. For the first time, interventions show the ability to lower beta-amyloid and tau in people, turning BAT Levels into an actionable target for prevention.
Sep 2024
Routine, lab‑agnostic BAT Testing protocol
removes analysis paralysis.
BATWatch developed the first agnostic testing protocol: a system that combines routine, annual testing and probability-based interpretation, instead of relying on any single test or manufacturer. This breakthrough made tracking BAT Levels accessible, accurate over time, and scalable for prevention, ending “analysis paralysis” and empowering patients to act now, not someday.
May 2024
BATWatch expands footprint to rest of USA.
Mar 2025
BATWatch surpasses 1,000 patients
600 completed BAT Pill protocol.
BATWatch surpasses 1,000 patient enrollments, with over 600 individuals completing BAT Pill treatment cycles as part of a rolling real-world evidence (RWE) study. Early results show the majority of treated patients achieve measurable reductions in Beta-Amyloid and Tau biomarkers, providing strong, practical support for the BAT Pill protocol as a tool for proactive brain health management.
May 2025
BATWatch provider network enrollment
surpasses 200 providers, throughout USA
and Canada.
BATWatch provider network surpasses 200 MDs and NPs, now delivering 100% nationwide coverage in the U.S. and 85% of Canada. Clinicians across North America are rapidly adopting and championing the BATWatch protocol, demonstrating widespread acceptance, real-world adaptation, and growing momentum behind proactive brain health for all.