MCI and AD Flashcards
Which presentation of MCI most frequently predates AD dx?
Amnestic MCI. Verbal memory impairment is most common, although some cases show greater visual memory impairment.
Are other forms of MCI possible?
Yes, although amnestic MCI is the most common, nonamnestic MCI can also predate dementia.
What percent of MCI cases convert to dementia per year?
10%
Discuss the model for preclinical AD.
Based on Clifford Jack’s work, including biomarker based data. Earliest pathological biomarkers include PET amyloid imaging, followed by accumulation of beta amyloid in CSF, and hippocampal volume loss. These changes would be observed prior to the onset of significant clinical symptoms.
What is DSM5 criteria for Mild or Major neurocognitive disorder for AD?
1) there is insidious onset and gradual progression of impairment in one or more cognitive domains
2) memory impairment is an early and prominent feature
3) the syndrome as a whole is not better attributed to other conditions.
Describe the neuropathology of AD?
Lesions of AD consist of synaptic and neuronal loss associated with progressive deposition of amyloid in the form of diffuse neuritic plaques along with accumulation of tau protein in the form of neurofibrillary tangles. Amyloid beta may clump together as early as 20 years prior to clinical disease onset. Tau changes occur as early as 15 years prior to clinical symptoms.
Research has shown that when amyloid beta is no longer properly cleared from the brain, it accumulates and can lead to neurodegeneration long before the first symptoms of Alzheimer’s disease (AD) start to become visible. This understanding of AD highlights the importance of early detection and diagnosis as a central component of future patient care.
A-beta starts to collect inside the brain. This may begin as many as 20 years before the first signs of AD appear. A-beta is produced inside the brains of all people, but in healthy people, it is removed by the body before it can cause harm. In the brains of people with AD, A-beta clumps together in bigger and bigger groups and forms clusters known as plaques. As time goes on, plaques begin to form in more and more parts of the brain, which are responsible for learning, memory and other tasks. The second process, involving tau protein, begins about 15 years before the first signs of AD appear. Tau normally plays a helpful role in the brain. However, in people with AD, tau becomes altered and forms tangles within nerve cells. Eventually, the processes involving A-beta and tau can injure nerve cells. As this injury affects one brain region after another, it leads to the appearance of symptoms you may recognize.
Over time, with cell loss, there is reduction in production and sensitivity to various neurotransmitters including choline aceyltransferase (enzyme responsible for the synthesis of the neurotransmitter acetylcholine), as well as serotonin and norepinephrine.
The neuropathological progression of the disease follows a temporal to frontal spread. The hippocampus and entorhinal cortex are implicated in the early stage of the disease, followed by the frontal, temporal, and parietal association areas with disease progression. It is in the temporal lobe and association areas where most atrophy occurs. Primary motor, visual, auditory, and somatosensory cortices as well as aspects of subcortical structures are relatively unaffected until quite late in the disease process.
AD is a disease that progresses over time, leading to worsening symptoms, and can ultimately cause death.
AD accounts for what percentage of all dementias?
60-80% of all cases of dementia
What are risk factors for AD?
1) Age, typically over age 60 is the single largest known risk factor.
2) Most AD cases are sporadic. However having a 1st degree family member with AD increases risk. Early onset AD associated with mutation on chromosomes 1 and 14 (presenilin genes) and 21 (APP gene). Chromosome 21 is also involved in Down Syndrome, and older adults with Down syndrome tend to develop plaques consistent with AD. Individuals with ApoE4 genotype on chromosome 19 have higher risk of developing AD.
3) Cardiovascular risk factors, such as high cholesterol
4) Mod to severe TBI
5) Diabetes mellitus (especially if poorly controlled)
6) History of depression
7) Concurrent small vessel disease
8) Lower education or cognitive reserve
What percentage of people over age 65 have AD symptoms?
5%, with prevalence rates increasing over time
What is the average age of AD dx?
About 75 years old
Which ethnicities are at greater risk for developing AD?
African Americans followed by Latin Americans are more likely to develop AD than Caucasians. Likely explained by increased prevalence of related medical conditions and factors such as education and access to healthcare.
What percent of AD cases have a familial variant?
About 5% of patients with AD have a familial variant. These are typically early onset and have more rapid decline, with symptoms presenting between ages of 40 to 60.
What percent of individuals older than 85 meet criteria for AD?
Between 25-50%
How do ppl die from AD?
complications or illnesses (aspiration, cardiovascular failure, pneumonia, decubitus ulcer)
What is the length of AD illness?
Ranges from 5 to 15 years, with mean duration of around 7 years.
How often is clinical diagnosis accurate based on comprehensive evaluation, including MRI, biomarker studies, neurological exam, NP eval, and careful history.
85-90% accurate
Is PET used clinically?
Yes, and can be helpful in differentiating AD from FTD.
Which cognitive abilities are more resistant to aging?
1) Vocabulary and verbal skills, reading skills
2) Simple attention
3) Basic arithmetic
4) Recognition memory and recalling story gist
5) Remote memory
Which cognitive skills normally decline with age?
1) Sustained and divided attention
2) Processing speed
3) Learning rates
4) How well one can spontaneously recall information
5) Mental flexibility
