BIO T8 Flashcards
(57 cards)
Which of the following is not a pharmacological treatment for Alzheimer’s disease?
a) Donepezil
b) Memantine
c) Rivastigmine
d) Metformin
D
Which class of drugs is commonly prescribed to alleviate symptoms of Alzheimer’s disease?
a) Antidepressants
b) Antipsychotics
c) Cholinesterase inhibitors
d) Anxiolytics
C
Which medication is an NMDA receptor antagonist used in the treatment of moderate to severe Alzheimer’s disease?
a) Donepezil
b) Rivastigmine
c) Memantine
d) Galantamine
C
What is the primary mechanism of action of cholinesterase inhibitors in Alzheimer’s disease treatment?
a) Blocking glutamate receptors
b) Enhancing cholinergic neurotransmission
c) Inhibiting serotonin reuptake
d) Increasing dopamine levels
B
Which of the following drugs is typically prescribed to manage behavioral symptoms such as agitation and aggression in Alzheimer’s patients?
a) Rivastigmine
b) Galantamine
c) Haloperidol
d) Memantine
C
What is the primary goal of combining Donepezil and Memantine in the treatment of Alzheimer’s disease?
a) To delay disease progression and improve cognitive function.
b) To reduce behavioral symptoms and agitation.
c) To prevent the formation of amyloid plaques in the brain.
d) To enhance neurogenesis and synaptic plasticity.
a
- Which stage of Alzheimer’s disease is typically targeted by the combination therapy of Donepezil and Memantine?
a) Mild cognitive impairment (MCI)
b) Early-stage Alzheimer’s disease
c) Moderate to severe Alzheimer’s disease
d) Advanced dementia
C
What is the ratio of glia and neurons?
Glia (etym. Glue of neurons old) outnumber neurons in the cerebral cortex, but neurons outnumber glia in several other brain areas (cerebellum)
Why is A-beta bad?
Misfolds and becomes sticky → clumbs to form oligemers → plaquesTrigger the release of cytokines because they’re observed by microglia → neural damage + synapse removal (phagocytosis)
What is the effect of oligimers
Weaken synaptic communication → might affect memory
What is neurodegeneration caused by Tau?
Tau (components of tangles) usually stablising the cytoskeletal transport → modified → abnormal shape + disconnected from the axon and moves towards the cell body → can spread to healthy neurons spreading tau’s malformation and neurodegeneration
What exactly causes the neural degeneration
excessive amounts of Amyloid beta in the cytoplasm of cells, not the external amyloid beta plaques → cytokines activated
Which chromosone has implicated in the production o amyloid beta?
21 chromosomes because people with down syndrome also have amyloid beta;
Under which conditions can amyloid-beta reproduce (Eisele et al., 2019)
After being boiled, steel still has hints of a-beta that can reproduce; even small scale
What is the amyloid beta hypothesis and related issues?
Extracellular a-beta accumulation triggers all pathological processes that culminate in AD → drugs targeting the secretase enzymes are not safe or effective
What is the Tau hypothesis and related issues?
Microtubule protein that causes neurodegeneration via breaking down axons and synaptic communication → effective treatments are challenging because of the complex AD pathology
What is the inflammation hypothesis and related issues?
Microglia + astrocytes → cytokines: using biomakerker treatments are complicated because they could interfere with the normal immune response
What is the cholinergic and oxidative stress hypothesis and related issues?*
Neuronal damage as a result of choline loss which uses acetylcholine → ACh esterase as symptomatic treatment but oxidative stress elevating components cannot be chemically bound to ACh-es
What is are new treatments suggested for AD?
Gut microbiome + Immune systemintestinal mucosal lymphoid tissue 70% - 80% of all immune cells in the body + first defence mechanismsCould also directly induce cytokine reaction, via GABA or via enteroendocrine cells that affect the brain through neuroimmune pathwaysCan affect neurotransmitter production and release (vagus nerve)
What is frontotemporal dementia?
= pick’s disease → genetic mutation that only causes NFTs and results in degeneration
of the frontal and temporal cortex → emotional changes and loss of executive functions (damaged prefrontal cortex), language disturbance (temporal lobe)
Explain the steps of AD pathogenesis?
Amyloid plaques extracellular beta-amyloid + degenerating axons and dendritesactivated microglia and reactive astrocytes, –> neuroinflammatory response produces cytokinesdestroy the degenerating axons and dendrites = only a core of beta-amyloid + neurofibrillary tangles consist of dying neurons that contain intracellular accumulations of twisted filaments of hyperphospholated tau protein –> leaves a trail of deformed and useless axons*
Which enzyme is responsible for what in AD?
a gene encodes the production of the ~-amyloid precursor protein (APP), a chain of approx imately 700 amino acids. APP i then cut apmt in two places by enzymes known as secretases to produce AP. TI, e first, P-secretase, cuts the ‘‘tail” off of an APP molecule. The second, y-secretase (gamma-secretase), cuts the “head” off. The result is a molec ule of AP that contains either 40 or 42 amino acids. The location of the second cut of the APP molecule by y-secretase determines which form is produced. In healthy brains, 90-95 percent of the Al3 molecules are of the short form; the other 5-10 percent are of the long form. In patients with Alzheimer’s disease the proportion of long Al3
Which brain region are affected by the neurodegeneration and how does an AD brain look?
the hippocampus entorhinal cortexneocortex (especially the association cortex of the frontal and temporal lobes)nucleus basalis locus coeruleus raphe nuclei
What is the other prevalence of AD?
10 percent of the population above the age of 6550 percent of people older than 85.
