Neurodegenerative Disorders Quiz

Cerebral cortex, basal ganglia, and hippocampus are typically the first brain regions affected in Alzheimer's Disease.

Common symptoms of Alzheimer's include dementia, memory loss, disorientation, mood changes, and communication difficulties.

A group of brain diseases characterized by progressive loss of neurons and brain function.

Focuses on the brain regions first affected during neurodegenerative disorders, the pathology of Alzheimer's disease (including biochemistry), risk factors for Alzheimer's, treatment of Alzheimer's, and the concept of prion diseases, including pathophysiology.

Characteristic proteins and genes linked to the affected brain regions.

Factors that increase the likelihood of developing Alzheimer's disease.

The drugs used to treat Alzheimer's disease.

Diseases caused by misfolded proteins that aggregate and cause brain damage.

Impairment of communication between neurons, disrupting cognitive function.

Inflammation in the brain, damaging neurons and worsening brain diseases.

A brain disorder with abnormal tau protein and possible memory loss.

Neurological disorder affecting movement, balance, and vision, progressing into dementia.

Dementia affecting behaviour, personality, and language, with Pick bodies.

Dementia affecting frontal and temporal lobes, and linked to Parkinson's-like symptoms.

Genetic link to frontotemporal dementia and Parkinsonism, impacting tau protein.

Early-onset Alzheimer's disease, with various genetic links.

A neurodegenerative disease affecting the basal ganglia and midbrain, causing slow movements, tremors, and rigidity.

A neurodegenerative disease affecting the basal ganglia (striatum), causing uncontrolled movements.

A neurodegenerative disease affecting motor neurons, leading to weakness and paralysis.

A neurodegenerative disease affecting the cerebral cortex, basal ganglia, and cerebellum, resulting in dementia and movement disorders.

Significant, progressive loss of intellectual abilities—memory, focus, and judgment—that severely interferes with daily tasks.

Abnormal protein folding that causes harmful aggregate buildup in neurons, implicated in neurodegeneration.

Symptoms of Alzheimer's disease include memory loss, confusion, personality changes, difficulty with routine tasks, disorientation, and eventually loss of speech, appetite, bladder/bowel control, and complete dependence.

Alzheimer's disease symptoms worsen over time, progressing from mild cognitive impairment (MCI) to severe stages, affecting various aspects of daily life.

Abnormal protein structures inside nerve cells in the brain, a hallmark of Alzheimer's disease.

Abnormal protein deposits outside nerve cells in the brain, another hallmark of Alzheimer's disease.

A protein in the brain that, when processed abnormally, can lead to the formation of beta-amyloid.

The buildup of beta-amyloid peptides, leading to the formation of amyloid plaques, a characteristic of Alzheimer's disease.

A peptide that leads to amyloid plaque formation in Alzheimer's disease.

Brain shrinkage (atrophy) occurs in Alzheimer's disease, impacting brain structure and function.

A protein that helps stabilize microtubules, which are important for transporting nutrients and other molecules within neurons.

A process where a protein has too many phosphate groups attached to it, changing its shape and function.

Small, soluble clumps of beta-amyloid that are particularly toxic to neurons.

An enzyme that cleaves APP in a way that leads to the production of β-amyloid. This is an abnormal processing of APP.

An enzyme that cleaves APP both in normal and Alzheimer's processing. It's involved in creating the abnormal Aβ1-42 form, which is amyloidogenic.

Referring to the formation of amyloid plaques, which are a hallmark of Alzheimer's disease.

Structures inside neurons responsible for transporting proteins and organelles. They are disrupted in Alzheimer's due to the abnormal phosphorylation of tau.

They are linked to each other in a vicious cycle. Amyloid plaques can induce tau pathology (causing tangles) and tangles can exacerbate amyloid aggregation.

When amyloid plaques and neurofibrillary tangles disrupt communication between neurons, causing problems with learning, memory, and thinking.

Immune cells (glia) in the brain become overactive, attacking neurons and causing more damage like a fire.

A genetic disorder where a specific gene causes abnormal tau protein, leading to dementia, personality changes, and Parkinson's symptoms.

Alzheimer's disease that starts at a younger age due to inherited genetic mutations.

Common symptoms of Alzheimer's include dementia, memory loss, disorientation, mood changes, and communication difficulties.

Alzheimer's disease is marked by the aggregation of two key proteins: amyloid-beta (Aβ) and tau.

Amyloid-beta (Aβ) is derived from a larger protein called amyloid precursor protein (APP). Abnormal processing of APP leads to the production of Aβ peptides that clump together, forming amyloid plaques.

Tau protein normally helps stabilize microtubules, which are important for transporting nutrients and other molecules within neurons. In Alzheimer's, tau becomes hyperphosphorylated, causing it to detach from microtubules and clump together, forming neurofibrillary tangles.

Risk factors for Alzheimer's Disease include age, genetics, family history, lifestyle factors (e.g., diet, exercise, smoking), and medical conditions (e.g., diabetes, high blood pressure).

Prion diseases are caused by misfolded proteins called prions. These prions can convert normal proteins into misfolded versions, leading to the formation of aggregates that damage brain cells.

The most common drugs used to treat Alzheimer's Disease aim to improve cognitive function, although they don't cure the disease. These include cholinesterase inhibitors (e.g., donepezil, rivastigmine) and memantine, which is an NMDA receptor antagonist.

Changes in the structure of the neuronal cytoskeleton, which is vital for keeping the neuron's shape, transporting important molecules, and communication within the cell. These changes can disrupt these essential functions and contribute to neurodegeneration.

An imbalance in the creation, folding, movement, and breakdown of proteins within a neuron. This imbalance is critical because proteins are essential for neuronal survival and function. Disrupted proteostasis is involved in neurodegenerative diseases.

A neurodegenerative disease characterized by memory loss, disorientation, mood changes, and communication difficulties. It's the most common form of dementia, affecting 60-80% of cases. Key pathological features include amyloid plaques and neurofibrillary tangles.

Caused by brain damage due to cerebrovascular disease, such as stroke or chronic ischemia. It accounts for 10-20% of dementia cases. Symptoms include impaired judgment, inability to plan, and stepwise decline in cognitive abilities.

Tau protein normally helps stabilize microtubules, which are like transport highways inside neurons, moving nutrients and essential materials.

In Alzheimer's, tau becomes hyperphosphorylated, meaning it gets too many phosphate groups attached, changing its shape and making it detach from microtubules.

Hyperphosphorylated tau forms twisted fibers that clump together inside neurons, creating tangled structures called neurofibrillary tangles.

Beta-amyloid (Aβ) is a fragment of APP that is produced when the protein is processed abnormally. It clumps together, forming amyloid plaques.

Amyloid plaques are clumps of Aβ that build up outside neurons. They disrupt cell function and cause inflammation.

Plaques can trigger a chain reaction, leading to the creation of neurofibrillary tangles. They also directly disrupt the function of neurons.

Amyloid plaques and neurofibrillary tangles create a vicious cycle where each worsens the other, leading to more neuronal damage.

The two hallmarks of Alzheimer's disease are neurofibrillary tangles and amyloid plaques. Neurofibrillary tangles are twisted fibers of a protein called tau inside nerve cells, while amyloid plaques are clumps of a protein called beta-amyloid outside nerve cells.

Amyloid precursor protein (APP) is a protein normally present in the brain. In Alzheimer's, it's processed abnormally, producing beta-amyloid peptides.

Beta-amyloid aggregation refers to the process where beta-amyloid peptides stick together to form clumps called amyloid plaques. This aggregation is abnormal and harmful to brain cells.

Brain atrophy, or shrinkage, in Alzheimer's is caused by the progressive loss of nerve cells (neurons) due to amyloid plaques and neurofibrillary tangles, disrupting brain structure and function.

Amyloid plaques can induce the formation of neurofibrillary tangles, and tangles can worsen amyloid aggregation, creating a vicious cycle of damage in the brain.

Neurofibrillary tangles disrupt the transport of nutrients and other vital molecules within neurons. They interfere with normal function and eventually lead to neuronal death.

Abnormal processing of APP leads to an increase in the production of beta-amyloid peptides. These peptides aggregate and form amyloid plaques, which are toxic to brain cells.

A peptide produced from the abnormal processing of the Amyloid Precursor Protein (APP), by β-secretase and γ-secretase enzymes. It forms amyloid plaques that are toxic to neurons and contribute to Alzheimer's disease.

A protein found in the brain that is normally processed in a way that doesn't lead to Alzheimer's disease. However, when processed abnormally, it can be broken down into β-amyloid, which is toxic.

They are enzymes that process APP. β-secretase cleaves APP in a way that leads to the production of β-amyloid, an abnormal processing. γ-secretase is involved in both normal and abnormal processing of APP.

Normally, tau helps stabilize the microtubule system, which is vital for transporting materials within neurons. However, in Alzheimer's, tau becomes abnormally phosphorylated (with too many phosphate groups), causing it to tangle. This disrupts microtubule function and leads to neuron death.

Both amyloid plaques and neurofibrillary tangles disrupt communication between neurons (synaptic dysfunction) and contribute to neuron death. This ultimately leads to cognitive decline.

The accumulation of β-amyloid, forming amyloid plaques, and the formation of neurofibrillary tangles contribute to brain atrophy (shrinkage) and cognitive decline. These changes underlie many of the symptoms of Alzheimer's disease.