Since you are at risk for both Parkinsons and Alzheimers, your competent? doctor should have EXACT PROTOCOLS TO PREVENT THAT OCCURENCE! Well, do those prevention protocols exist, or not?
DOES YOUR DOCTOR HAVE EXACT DEMENTIA PREVENTION PROTOCOLS? NO? So, your doctor is incompetent?
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.`
3. A 20% chance in this research. July 2013.
4. Dementia Risk Doubled in Patients Following Stroke September 2018
Parkinson’s Disease May Have Link to Stroke March 2017
Alzheimer’s and Parkinson’s Share Hidden Early-Stage Signals
Despite their differences, Alzheimer’s disease and Parkinson’s disease share several risk factors and mechanisms of neuronal damage. Both also feature a phase that precedes the appearance of symptoms — a possible therapeutic window during which interventions could reduce the risk for neurodegeneration or slow its course.
At the 55th Congress of the Italian Society of Neurology in Padua, Italy, specialists discussed recent advances in identifying this preclinical phase and strategies for managing it.
Alzheimer’s Disease: Assessing, Communicating, and Reducing Risk
“In an updated version of the diagnostic criteria for Alzheimer’s disease, the International Working Group (IWG) has clearly defined the characteristics of the stage preceding the clinical onset of neurodegeneration and outlined the possible trajectories of patients who show no cognitive deficits but test positive for amyloid plaques and tau protein accumulations,” explained Giovanni Frisoni, director of the Memory Clinic at Geneva University Hospitals, Geneva, Switzerland.
“The IWG describes a continuum that includes a presymptomatic risk phase, a prodromal phase, and a stage marked by mild, moderate, or severe dementia,” Frisoni said. “Once dementia is established, intervention can only affect the rate of progression. Monoclonal antibodies targeting amyloid plaques can slow degeneration but not stop it. In the presymptomatic phase, however, we can still ask whether a patient will develop cognitive impairment. We therefore need clear criteria to estimate an individual’s risk and to guide preventive strategies.”
A recent study involving adults aged 65-77 years who underwent PET imaging to detect amyloid plaques and tau deposits found that those without cognitive impairment but positive for both biomarkers had a 60% likelihood of developing Alzheimer’s disease symptoms within 6 years. “During evaluation, beyond amyloid and tau findings and patients’ subjective perception of cognitive changes, we must also consider numerous other risk factors,” Frisoni noted. “The degree of risk should then be communicated appropriately to the patient, followed by a preventive strategy to mitigate it.”
According to the 2020 report by The Lancet Commission on dementia prevention, intervention, and care, approximately 45% of dementia cases are linked to modifiable risk factors such as lifestyle, physical activity, diet, alcohol use, environmental pollution, stress, and head trauma.
“These are the levers we can act on preventively,” Frisoni said. “Of course, the ability to modify them varies — not everyone can relocate to a less polluted area or meaningfully reduce daily stress.”
He added that research is now underway to assess the potential benefits of monoclonal antibody therapy in the presymptomatic phase, where intervention might prove most effective.
Parkinson’s Disease: Early Warning Signs
“Unlike Alzheimer’s disease, Parkinson’s affects multiple organs and body systems, producing symptoms such as tremors, loss of smell, muscle stiffness, slowed movement, and urinary urgency,” said Angelo Antonini, MD, PhD, professor of neurology at the University of Padua, Padua, Italy.
According to a hypothesis proposed by Danish neurologist Per Borghammer, Parkinson’s disease may originate differently depending on the individual. In some patients, the disorder begins with alpha-synuclein aggregates forming in the central nervous system — a mechanism referred to as brain-first. In others, it starts in the peripheral nervous system, particularly in the enteric (gut) nervous system, before spreading to the brain — a pattern known as body-first.
In the brain-first form, early symptoms are motor related, such as tremor and bradykinesia (slowness of movement). In the body-first form, gastrointestinal disturbances and REM sleep behavior disorders often appear years before motor symptoms develop.
“A recent Italian study confirmed this diversity in early manifestations among 400 patients — some experienced REM sleep disturbances, constipation, and loss of smell before any motor symptoms emerged,” Antonini said. “For certain individuals, these three signs indicate an increased risk of Parkinson’s and may appear years, or even a decade, before tremor begins. Another key factor to consider is family history, which carries more weight in Parkinson’s than in Alzheimer’s disease.”
At present, alpha-synuclein deposits cannot be detected with PET imaging, Antonini noted. However, EEG can identify compensatory brain reorganization processes that occur in early degeneration, while functional MRI can help assess cognitive decline.
“Once these early warning signs are recognized, what can we do?” Antonini asked. “Several compounds are currently under development for use in the early stages of Parkinson’s. Drugs already effective in other neurodegenerative diseases — such as monoclonal antibodies targeting amyloid plaques — may also have potential, since amyloid pathology can be present in some Parkinson’s cases as well.”
This story was translated from Univadis Italy, part of the Medscape Professional Network.
