Early stage screening of Alzheimer's disease by detecting subtypes of MCI...with a normal webcam POC.
A reliable and inexpensive diagnostic test that can be used in any doctor's office all over the world....
AI 4.0...A decision making tool for GP's ( General Practitioner ) Nature.com
It is not realistic that we shall have a cure before 2025 for Alzheimer's disease : Forbes 2018
There are about 112 agents in the current Alzheimer's treatment pipeline...if you can't monitor...it is WASTE MONEY
Before the first symptoms of Alzheimer's disease appears some alternations in the brain can cause little changes in eye movement patterns, gait patterns, face recognition patterns...AI can recognize these changes early and identify patients at risk of developing the most severe forms of dementia. AI see some changes that humans can't see ( even it's too complex) but can also monitoring the patient and whith these patterns the doctor can follow the progression and efficiency of his treatment or prevention therapy. Also for patients who have already AD doctors can use the device for adjustments. When a doctor or radiologist reads scans from PET,MRI it is impossible wheter a person will progress AD or dementia and his subtypes. AI can also predict the severity of the disease in different patients. For drug companies it is very difficult to identify the wright patient. With computational pathology and pattern recognition technics we can make better diagnosis and less misdiagnosis.
THERE IS A BIG DIFFERENCE BETWEEN A BIOLOGICAL BIOMARKER FOR ALZHEIMER'S DISEASE AND A DIGITAL BIOMARKER...
Biological Biomarker for Alzeimer's: can be a toxic protein like amyloid or TAU
Digital biomarker: can give you data about the function of different parts of your brain
Only with digital biomarkers you can make a differentation between Alzheimer's disease and other neurodegenerative diseases preclinical...like Lewy Body dementia with 80% misdiagnosis and 50% get a diagnosis of Alzheimer's disease
The reason why 99,6% of all Alzheimer's drugs fail...even with neurons without any plaques...we still have an old neuron with low neuroplasticity and low communication...New neurons Archive Old memories...
Imaging biomarkers (PET imaging of amyloid and tau aggregates) and CSF markers (measurement of amyloid and tau) are very helpful to identify AD pathophysiology, but are unlikely to be a routine diagnostic tool: PET technique is only accessible in specialized departments and is very expensive; lumbar puncture may be regarded as invasive, complicated, and time consuming by many physicians.
The hope is to diagnose Alzheimer’s disease before the symptoms start. Future treatments could then target the disease in its earliest stages before irreversible brain damage or mental decline occurs. The development of marker panels is in its early stages and requires further substantial preclinical and clinical validation. It seems likely that only a combined analysis of several biomarkers will define a patient-specific signature to diagnose AD in the future. The respective diagnostic and prognostic markers of AD are expected to improve patients’ outcome significantly and to support the discovery of new treatment targets. Compared with neuroimaging or collection of CSF, it is important for biomarkers to be cost-effective and time consuming.
It is important to identify more specific and more sensitive AD biomarkers that can not only accurately diagnose early-stage AD but also differentiate AD from non-AD dementias (vascular dementia, tauopathy, frontotemporal dementia, Lewy body dementia, etc.). These biomarkers should be able to assess the risk of AD in combination with other known risk factors, facilitate screening of potential therapeutic agents and their identification, track the prodromal stages of AD, guide therapeutic decision-making, and monitor therapeutic efficacy
Blood based biomarkers and retina scans
With ultrasensitive assays we can detect beta-amyloid peptide ratios and peptide secondary structure in blood that correlate with brain and CSF amyloid. Till know we have no other specific markers blood based beside amyloid...to make a differentiating between AD and non-AD dementias we need more specific blood based markers. We see the same problems with eye scans (retina scans)...we can detect only beta-amyloid...
With digital biomarkers we can differentiate AD from non-AD dementias...like vascular dementia, frontotemporal dementia, Lewy Body dementia, Parkinson...if we have enough different digital biomarkers and with AI,ML and DL we can make a differentation.
Mild Cognitive Impairment or MCI
MCI causes a slight but noticeable and measurable decline in cognitive abilities, including memory and thinking skills. Long-term studies suggest that 15-20 percent of the aged 65 and older may have MCI. There is a difference between normal aging cognitive decline and MCI. With all kind of rating scales it is not possible to see any difference.
Biomarkers for Alzheimer's disease can be really measured to indicate the presence or absense of the disease. For AD there is only one biomarker accepted amyloid beta. Preclinical b. amyloid as biomarker is difficult and very expensive to detect and it is only possible in hospitals. Digital biomarkers can be used outside the hospital POC ( in the waiting room or at home).
Blood glucose levels are a biomarker for diabetes and blood cholesterol for heart disease.
Accurate diagnosis is needed for Dementia Lewy Body
Dementia with Lewy Bodies (DLB) may account for up to 30% of all dementia cases. The symptoms of DBL can be difficult to disentangle from other dementia subtypes. DLB is characterized by a build-up of abnormal proteins (Lewy bodies) in areas that control cognition, movement, allertness and behavior.
Eye tracking ( saccadic eye movement tracking) and EEG are very sensitive digital biomarkers to make an accurate diagnosis.
AD and DLB pathologies often overlap within individuals. An individual is diagnosed with Parkinson disease dementia ( PDD) or DLB depends on the timing of symptoms onset. In dementia with Lewy Bodies, cognitive decline occurs within one year of the onset of movement disorder symptoms.
DLB is sensivity to antipsychotic drugs. We see also REM behavior disorder. Visual hallucinations and fluctuations in cognition, attention and allertness.
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These are the most commonly misdiagnosed conditions.
It is a degenerative disorder of the central nervous system with symptoms including tremors in hands, arms or legs, stiff muscles, and problems with balance or walking.
However, it is commonly mistaken for Alzheimer’s disease, stroke, stress, a traumatic head injury and essential tremor.
The condition causes an overactive thyroid gland, and is the most common cause of hyperthyroidism.
Symptoms include eyes bulging, anxiety, sweating, rapid pulse, unplanned weight loss or gain, and extreme tiredness.
Without treatment, it can prove life-threatening, however it is often mistaken for depression, ageing and under-exercising.
It is a chronic arthritis-like disorder characterised by widespread pain.
However, symptoms - anxiety, sensitivity to pain and incapacitating fatigue - can be confused with rheumatoid arthritis and chronic fatigue syndrome.
Normal pressure hydrocephalus
It is a build-up of cerebrospinal fluid in the brain that most commonly occurs after a stroke or ahead injury from a fall.
Symptoms of unsteady gait, progressive dementia and urinary problems, can be interpreted as Alzheimer’s disease or Parkinson’s disease.
The progressive autoimmune disease that attacks the central nervous system has symptoms including muscle spasms, lack of coordination, balance problems, blurred vision and cognitive impairment.
However, it is commonly mistaken for a viral infection, lupus, Alzheimer’s disease and bipolar disorder.
It is an autoimmune disorder marked by an inability to digest gluten, a protein in wheat, rye and barley.
Symptoms can include vomiting, abdominal pain and bloating, diarrhoea, weight loss, anaemia and leg cramps.
However it can be mistaken for irritable bowel syndrome, Crohn’s disease and cystic fibrosis
Chronic fatigue syndrome
The complex disorder has no known cause but symptoms include loss of memory or concentration, a sore throat, painful lymph nodes in neck or armpits, unexplained muscle or joint pain and extreme exhaustion.
It is often confused with sinus problems, hepatitis, fibromyalgia, lupus and rheumatoid arthritis.
It is a chronic inflammatory disease, with symptoms including fatigue, kidney, heart and lung damage, rash and joint pain.
However, it can be mistaken for chronic fatigue syndrome, fibromyalgia and rheumatoid arthritis.
This is where a tear develops in the aorta, the largest blood vessel branching from the heart, which causes the inner and middle layers to separate.
Symptoms can include sudden chest or upper back pain, loss of consciousness, shortness of breath, sweating and weak pulse in one arm.
However it can be misdiagnosed as heartburn, heart attack and stroke.