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True or False: Dementia is normal aging.

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True or False: Dementia is normal aging.

FALSE

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synpatic plasticity

the ability of synapses to strengthen or weaken in response to activity

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cognitive decline in aging brains

-Slower reaction time -Lower attention levels -Slower processing speeds -Decreased sensory/perceptual function -Changes in sleep pattern

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factors of brain aging

genetics (family history), education level, sleep time

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combined theory of aging

ROS production, DNA damage, mitochondrial damage

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neurogenesis

the development of new neurons

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occurence of neurogenesis

subventricular zone and subgranular zone

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factors that increase neurogenesis

environmental enrichment, exercise

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factors that decrease neurogenesis

aging, depression, physical disease

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ways to delay cognitive decline

-Minimizing stress -Exercise -Active social life -Diet (Omega 3 fatty acids, antioxidants, less sugar) -Higher education

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Parabiosis

the anatomical joining of two individuals, especially artificially in physiological research

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types of parabiosis

isochronic (young-young, old-old) and heterochronic (young-old)

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regarding parabiosis, research showed that (young/old?) blood impaired young subject performance of mice.

old

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regarding parabiosis, research showed that (young/old?) blood reversed age related impairments in cognitive function in old mice.

young

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dementia

loss of cognitive abilities/memory

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symptoms of dementia

-Difficulty with everyday tasks -Confusion in familiar environments -Difficulty with words/numbers -Memory loss -Changes in mood/behavior

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types of dementias

-Multi-infarct dementia -Fronto-temporal dementia -Alzheimer's disease

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mild dementia characteristics

-Retains judgment -Can sustain daily activities -Work/social life is impaired

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moderate dementia characteristics

-Independent living becomes hazardous -Requires some supervision

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severe dementia characteristics

-Requires constant supervision

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Aphasia

Loss of ability to understand or express speech

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Apraxia

Inability to link skilled motor movements to ideas or representations

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Agnosia

Deficit in recognizing objects that occurs in the absence of deficits in sensory processing

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Acalculia

The inability to perform simple mathematical calculations the patient previously knew

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cortical dementia

Co-occurrence of many cognitive deficits (Aphasia, Apraxia, Agnosia, Acalculia, Visuospatial deficits, Memory problems)

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subcortical dementia

Personality changes, Attention deficits, Slowness in cognitive processing, Difficulties with tasks requiring strategy

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Mixed Dementia

Both cortical and subcortical involvement, Patterns of cognitive performance midway between cortical and subcortical types

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non-vascular dementia categories (molecular classification)

-Amyloid-β (Aβ) -Microtubule-associated protein tau -TAR DNA-binding protein 43 (TDP-43) -Fused in sarcoma (FUS) -Α-synuclein -Prion protein

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Alzheimer's disease causes

gene mutations (Presenilin 1 (C14), Presenilin 2 (C1), Trisomy 21 (C21), Amyloid precursor protein (C21))

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__ million people nationally have Alzheimer's disease.

5.6

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__ is the state with the most Alzheimer's cases (670,000)

CA

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Fronto-temporal dementia is associated with the shrinkage of the _______ and __________ lobes.

frontal; temporal

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symptoms of FTD

-Impulsive -Inappropriate social behaviors -Neglect of personal hygiene -Repetitive/compulsive behavior -Speech problems

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types of FTD

behavioral variant FTD, semantic dementia, progressive nonfluent aphasia

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Lewy body dementia symptoms

-Bradykinesia (rigidity) -Recurrent and well-formed hallucinations -Memory deficits less severe than AD, but visuospatial deficits more severe than AD

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vascular/multi-infarct dementia (MID) is caused by...

blockages in the brain's blood supply

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risks for MID

-High blood pressure -Diabetes -High cholesterol -Family history of heart problems -Obesity -Smoking

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Parkinson's disease neuropathology

degeneration of dopamine-producing neurons in the brain

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neuropsychiatric symptoms of PD

-Executive dysfunction -Memory deficits -Attention deficits -Mood disturbances -Visuospatial deficits -Impulsivity

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treatment for PD

levodopa, deep brain stimulation, lesions

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brain changes resulting from AD

-Shrinkage of brain (Loss of neurons) -Decrease in volume of gray matter and white matter -Enlargement of lateral ventricles

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amyloid plaques

Insoluble extracellular deposits which accumulate in the cortex and hippocampus

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neurofribrillary tangles

Bundles of insoluble helical fibers within neurons

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Neurofribrillary tangles in AD are composed of abnormal ___ proteins

tau

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functions of tau in microtubules

-organize cytoplasm -serve as tracks of transport

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Separation of tau from microtubules results in disruption of connection and _______ ______

neuronal death

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ABC score

Measure severity of amyloid plaque in AD (Stage A, B, and C)

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BRAAK staging

Measure severity of tangles in AD (Stages 1-6)

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Plaque and tangles in AD causes hyperactivity of ________ and __________, which can cause brain damage

microglia; astrocytes

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50

Activation of the ______ system accompanies AD pathology

immune

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51

PET scans of patients with AD showed reduced...

brain glucose metabolism

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52

True or False: MRIs of AD patients show brain shrinkage.

TRUE

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type of medication for AD

-Acetylcholinesterase inhibitors (increases acetylcholine in synapses) -NMDA receptor antagonist (reduces glutamate excitotoxicity)

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risks for AD

-Age -Genetics (APP, PS-1, PS-2, ApoE4) -Head trauma -Diabetes -Stroke -High blood pressure -High cholesterol -Heart disease

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Ways to prevent AD

-physical exercise -social/leisure activity -higher education

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56

________ _______ accounts for the majority of dementia cases among people age 65+

Alzheimer's disease

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symptoms of AD

-Gradual memory loss -Decline in ability to perform routine tasks -Disorientation -Difficulty in learning -Loss of language skills -Impairment of judgment/planning -Personality changes

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____ is the primary risk factor of AD

age

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2/3 of people with Alzheimer's are ________.

women

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60

True or False: White Americans are more likely to have AD.

FALSE (Black Americans 2 times as likely; Hispanic Americans 1.5 times more likely)

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mild AD

-Loss of recent memory -Faulty judgment -Personality changes

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moderate AD

-Aggression -Agitation -Wandering -Sleep disturbances -Delusions

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severe AD

-Loss of all reasoning -Bedridden -Communication disability

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Mild Cognitive Impairment (MCI)

Measurable/greater-than-normal memory impairment detected with standard memory assessment tests (Normal general thinking and reasoning skills, Maintained ability to perform normal daily activities)

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Antipsychotics are used to treat _/__ in AD.

Agitation/Delusions

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SSRIs/SNRIs are used to treat ___________ in AD.

depression

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67

CNS stimulants are used to treat ________ in AD.

apathy

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Non-benzo hypnotics are used to treat ______ ___________ in AD

sleep disturbance

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Hyperphosphorylated tau

insoluble and dysfunctional, leading to tangles and microtubule destabilization

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Tauopathies

A class of neurodegenerative diseases associated with the pathological aggregation of tau protein in the human brain.

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primary tauopathy

Diseases which have Tau pathology as primary pathology (ex. Chronic traumatic encephalopathy, Frontotemporal Lobar Degeneration)

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secondary tauopathy

Disease which have Tau pathology as as well other major pathologies (ex. Alzheimer's disease)

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73

6 major isoforms of tau in the brain

3R causing FTD, 4R causing CBD, 4R causing PSP, 3R and 4R causing CTE, 3R and 4R causing AD

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74

Chronic Traumatic Encephalopathy (CTE)

a progressive, degenerative condition involving brain damage resulting from multiple episodes of head trauma

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CTE is typically found in...

-Boxers/professional fighters -Amateur/professional wrestlers -Football and rugby players -Ice hockey players -War veterans with history of blast or concussive injury

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signs of CTE (brain)

enlarged ventricles, shrinkage of brain matter

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pathological features of CTE

-Neurofibrillary tangles -Changes in white matter -Glial degeneration

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subtypes of frontotemporal degeneration

-Progressive nonfluent aphasia (affects left frontal lobe first) -Semantic dementia (affects left anterior temporal lobe first) -Behavioral variant Frontotemporal dementia (affects right frontal lobe first)

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Progressive nonfluent aphasia symptoms

-Hesitant/effortful speech -Speech apraxia -Stutter -Anomia -Phonemic paraphasia -Agrammatism

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semantic dementia symptoms

Loss of semantic knowledge

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behavioral variant FTD symptoms

-Deficits in emotional processing and behavioral/moral reasoning -Inappropriate behaviors in public -Compulsive behaviors -Regression to child-like state of reasoning

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__% of people with FTD have a family history of related dementia

~40

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neuroinflammation due to BV-FTD

-Chronic cortical inflammation -Microglial activation and dystrophy -Astrogliosis -Neuron death/neurodegeneration

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84

_________ _______ is the 2nd most common neurodegenerative disease

Parkinson's disease

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motor symptoms of PD

-Tremors -Stiffness -Impaired balance -Bradykinesia -Vocal symptoms -Difficulty walking -Dystonia

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non-motor symptoms of PD

-Hyposmia -Sweating and melanoma -GI issues -Pain

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87

Sporadic form of PD accounts for ~__% of cases

90

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Diagnosis of PD typically cannot be made until the onset of _____ symptoms.

motor

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89

Loss of neurons that produce _________ in the substantia nigra is the primary cause of PD.

dopamine

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functions of dopamine

-Behavior and cognition -Voluntary movement -Motivation -Punishment/reward system -Working memory and learning -Sleep, mood, attention

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There is a linear correlation between age of PD onset and time of -______ aggregate appearance.

a-synuclein

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Unfolded/disordered alpha-synuclein forms ____ ______.

lewy bodies

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Genetic mutations associated with PD affect either the cellular function of __________ or ___________

mitochondria; proteasomes

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_, _____, and ____ are genes associated with PD

DJ-1; Parkin; Pink1

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animal models used for PD

cell based assays, worm, fruit fly, zebrafish, rodents, non-human primates

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drugs used to treat PD

-Levadopa/L-Dopa (immediate precursor to dopamine) -L-deprenyl (inhibitor of MAO-B, an enzyme that degrades dopamine)

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deep brain stimulation

Surgeons implant electrodes into a specific part of the patient's brain. The electrodes are connected to a generator implanted in the chest near that sends electrical pulses to the brain.

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therapies to treat PD

-Deep brain stimulation -Mitochondrial/antioxidant-based treatments -Synuclein-based therapies (Vaccination, Compounds that inhibit aggregation) -Cell transplants (Stem cells)

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99

Huntington's disease is a(n) _________ _________ disease, meaning an affected person has a 50% chance of passing it on to children.

autosomal dominant

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100

Polyglutamine diseases are characterized by the expansion of the ___ repeat.

CAG

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