The Aging Nervous System And Dementia

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2 most common etiologies for dementia

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alzheimer's disease
cerebrovascular disease

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safety factor

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protective excess of brain cells which must be lost before symptoms of dementia start to develop

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neuritic plaques

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extracellular spherical lesions with a central core of beta-amyloid protien
in temporal lobe in hippocampus and para hippocampus

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neurofibrillary tangles

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Neurofibrillary tangles are pathological protein aggregates found within neurons in cases of Alzheimer's disease.
tau protein
wide spread through cortex
can be found to much lesser degree in normal aged brains

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DSM-IV Criteria for Dementia

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memory impairment (short-term memory impairment is a feature of the disease)
aphasia
praxia
agnosia
disturbance is executive functioning

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alzheimer's disease is

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coritcal dementia

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subcortical demensia

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Subcortical dementia refers to a clinical syndrome characterised by slowing of cognition, memory disturbances, difficulty with complex intellectual tasks such as strategy generation and problem solving, visuospatial abnormalities, and disturbances of mood and affect. The syndrome was first described by Kinnier Wilson, but further progress in development of the concept has occurred only within the past ten years. Subcortical dementia occurs in degenerative extrapyramidal disorders and has also been identified in inflammatory, infectious, and vascular conditions. Histologic, metabolic, and neurochemical investigations implicate dysfunction primarily of subcortical neurotransmitter systems and subcortical structures or subcortical-frontal connections in the genesis of the syndrome. Subcortical dementia contrasts neuropsychologically and anatomically with disorders such as dementia of the Alzheimer type that affect primarily the cerebral cortex. The clinical characteristics of subcortical dementia reflect the interruption of fundamental functions (motivation, mood, timing, arousal) mediated by phylogenetically and ontogenetically early maturing structures.

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diseases with subcoritcal dementia

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degenerative: parkinson's, huntington's, & progressive supranuclear palsy
Vascular: lecunar state, thalamic infarction
MS, HIV-associated dementia, normal pressure hydrocephalus

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Reversible toxic and metabolic causes of confusion in elderly (rule out before dementia diagnosis)

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electrolyte disturbances
hypothyroidism
vit. B12 deficiency
drug toxicity

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lewy bodies

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confined to brainstem in parkinsons
in cortex in dementia

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Lewy bodies

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Lewy bodies are abnormal aggregates of protein that develop inside nerve cells in Parkinson's disease (PD) and some other disorders. They are identified under the microscope when histology is performed on the brain.

Lewy bodies appear as spherical masses that displace other cell components. There are two morphological types: classical (brain stem) Lewy bodies and cortical Lewy bodies.

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dementia with lewy bodies symptoms

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visual hallucinations
parkinsonism: tremor, short shuffling gait
periods of fluctuating cognition

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hyperorality

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A condition characterized by insertion of inappropriate objects in the mouth

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Frontotemporal dementia

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prominent changes in personality, judgement, and behavior
-decline in personal hygeine
-mental rigidity & inflexibility
-hyperorality & dietary changes
-perseverative and stereotyped behavior
-impaired judgement

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frontotemporal dementia

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frontal & anterior temporal atrophy

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Lewy bodies

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Lewy bodies are abnormal aggregates of protein that develop inside nerve cells in Parkinson's disease (PD) and some other disorders. They are identified under the microscope when histology is performed on the brain.

Lewy bodies appear as spherical masses that displace other cell components. There are two morphological types: classical (brain stem) Lewy bodies and cortical Lewy bodies.

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dementia with lewy bodies symptoms

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visual hallucinations
parkinsonism: tremor, short shuffling gait
periods of fluctuating cognition

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hyperorality

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A condition characterized by insertion of inappropriate objects in the mouth

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Frontotemporal dementia

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prominent changes in personality, judgement, and behavior
-decline in personal hygeine
-mental rigidity & inflexibility
-hyperorality & dietary changes
-perseverative and stereotyped behavior
-impaired judgement

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frontotemporal dementia

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frontal & anterior temporal atrophy

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Pick body

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Pick bodies are tau (TAU)-positive cytoplasmic neuronal inclusion and are the pathological hallmark lesions of Pick disease, a neuropathological subtype of tau-postive frontotemporal dementias (FTDs).

Pick bodies are not related to the Lewy bodies observed in Parkinson disease, which are tau-negative and α-synuclein-positive (SYNA).

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Pick's disease

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Pick's disease is a rare and permanent form of dementia that is similar to Alzheimer's disease, except that it tends to affect only certain areas of the brain.
Causes

People with Pick's disease have abnormal substances (called Pick bodies and Pick cells) inside nerve cells in the damaged areas of the brain.

Pick bodies and Pick cells contain an abnormal form of a protein called tau. This protein is found in all nerve cells. But some people with Pick's disease have an abnormal amount or type of this protein.

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NINCDS-ADRDA Criteria Probable Alzheimer's Disease

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dementia
deficits in 2 or more cognitive areas
progressive worsening of memory and other cognitive functions
no disturbance of consciousness
onset between 40 & 90 years of age
absence of other systemic disorders
progressive worsening of cognitive symptoms
impaired activities of dailyliving
associated behavioral abnormalities

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location of amyloid plaques

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cerebral cortex
hippocampus
rarely in cerebellar cortex

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neurofibrillary tangles

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paired helical filaments containing hyperphosphorylated tau
located in association cortex, hippocampus NOT in cerebellum or spinal cord

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The amyloid hypothesis

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According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis
accumulate with advancing age in neuritic plaques
composed of B-A4 protein

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amyloid deposition precedes

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development of clinical dementia

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B-amyloid protein is produced

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from precursor protein coded for by 21st chromosome

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some cases of Alzheimer's disease are linked to

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genetic mutation on 21st chromosome

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all down syndrome patients

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develop alzheimer's by their 40s due to over expression of beta-amyloid precursor protein

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trisomy 21

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Down' syndrome

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B-A4 arises from

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B-APP gene on chromosome 21

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Presenilins

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Presenilins are a family of related multi-pass transmembrane proteins that function as a part of the gamma-secretase protease complex. Vertebrates have two presenilin genes, called PSEN1 (located on chromosome 14 in humans) that encodes presenilin 1 (PS-1) and PSEN2 (on chromosome 1 in humans) that codes for presenilin 2 (PS-2).

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Presenilins & Alziemher's

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n patients suffering from Alzheimer's disease (autosomal dominant hereditary), mutations in the presenilin proteins (PSEN1; PSEN2) or the amyloid precursor protein (APP) can be found. The majority of these cases carry mutant presenilin genes. An important part of the disease process in Alzheimer's disease is the accumulation of Amyloid beta (Aβ) protein. To form Aβ, APP must be cut by two enzymes, beta secretases and gamma secretase. Presenilin is the sub-component of gamma secretase that is responsible for the cutting of APP by gamma secretase.

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PS1 & PS2

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mutated forms on chromosomes 14 and 1 cause increased secretion of b-amyloid and can lead to early-onset familial AD

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Apolipoprotein E

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Apolipoprotein E (APOE) is a class of apolipoprotein found in the chylomicron and IDLs that binds to a specific receptor on liver cells and peripheral cells. It is essential for the normal catabolism of triglyceride-rich lipoprotein constituents.[1

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APOE-2

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maybe protective against AD

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APOE-4

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associated with increased risk of AD

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50% of AD patients

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have the allele 4 for apolipoprotein

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APOE

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is found in B-amyloid plaques & neurofibrillary tangles and may affect protein-protein interactions

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chromosome 21

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amyloid precursor - beta amyloid plaques

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chromosome 1 & 14

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produce presenilin - secretases - beta amyloid plaques

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chromosome 19

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apollpoprotien - neurofibirllary tangles & neurtic plaques

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decreased Ach in AD

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amygadala & hippocampus have highest density of cholinergic axons

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early pathology of AD

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hippocampus
progresses to cortical areases

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areas of brain not involved in alziehmer's pathology

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primary motor/parietal cortex
visual areas/occipital cortex

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choline acetyltransferase

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catalyzes formation of Ach from acetyl-CoA & choline

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Ach is broken down into choline and acetate by

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acteylchoninesterase or butyrylcholinesterase

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In AD deficiency of Ach in

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nucleus basalilis

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In AD deficiency of serotonin in

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raphe nuclei

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In AD their is a deficiency of catecholamines in

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locus ceruleus

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In AD their is a defciency of somatostatine, GABA, glutamate, and aspartate in

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cerebral cortex

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Vascular Dementia

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associated with stroke and cerebrovascular disease

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Binzwanger's encephalopathy

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diffuse or confluent ischemia in subcortical white matter, often associated with lacunar strokes

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lacunar state

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multiple small infarctions related to ischemia of small penetrating vessels, located in subocortical white matter, thalami, and basal ganglia

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left hemisphere stroke causes

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language deficits

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temporolimbic area stroke causes

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memory deficits

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Multi-Infarct Dementia
(DSM-IV)

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presence of dementia syndrome
stepwise course with patchy cognitive symptoms
focal neurologic signs and symptoms
evidence of contributing cerebrovascular disease

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stroke risk factors

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hypertension, cardiac diseases that are a source of emboli (atrial fib, MI, valvular disease), DM, arterial vascular disease (atheroscelrosis, vasculitis)

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4 cholinesterase inhibitors approved for alziehmer's

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tacrine
donepezil
rivastigmine
galantamine