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Printable Handouts
Navigable Slide Index
- Introduction
- Jeanne Calment
- Alzheimer prevalence increases with aging
- Clinical dementias in the elderly
- Cortical atrophy in AD
- Brain aging begins by age 30
- Gray matter loss rates in healthy aging and AD
- Neocortical regions thinned with age
- Synapse loss in normal aging human cortex
- Striatal dopamine receptors show progressive loss
- Normal aging: neuron atrophy without neuron loss
- Cerebral cortex: astrocytes increase progressively
- Entorhinal cortex neuron loss in earliest AD stages
- Functional model for AD, synapse loss, and aging
- Eye-blink conditioning declines during middle-age
- EEG and aging
- Broad cognitive ability peaks before 30 in US
- Verbal memory declines after age 20
- No age decline in axonal conduction speed
- Dual task performance declines during aging
- Stages of AD, Clinical Dementia Rating (CDR)
- Age-specific population frequencies
- APOE shifts amyloid disposition to an earlier age
- Different pathways lead to different outcomes
- Alzheimer-type changes are common in aging
- Human brain amyloid increase with age
- Amyloid hypothesis of AD
- Neurofibrillary tangles (NFT)
- Aging and increasing Braak stage in Alzheimer
- Braak stages
- Non-invasive assessment of tau pathology
- Grafted neuron show PD-like changes
- Alzheimer and Parkinson's diseases
- Neurodegenerative a-synucleinopathy in mice
- Grafted dopaminergic neurons in aging rats
- Glial roles in synaptic atrophy during normal aging
- Increased GFAP-containing intermediate filaments
- Experimental studies of aging astrocytes
- Synapse density & blood flow vs astrocyte volume
- Modest AD-like changes in aging monkeys
- Chromosomal genes in AD
- ApoE alleles and AD risk
- ApoE4 faster cognitive decline (MMSE)
- ApoE alleles determine entorhinal cortex thickness
- ApoE4 carriers accumulate amyloid earlier
- Risk factors for cognitive decline & dementia
- Low SES-education increases risk of AD
- Environmental exposures & risk for AD
- Los Angeles Basin - 7 year follow-up
- Components of air pollution and cognitive function
- Traffic related particulate impairs cognitive function
- Alzheimer drug trials: no winners
- Anti-amyloid treatment in asymptomatic AD
- Future goals to optimize brain aging
Topics Covered
- Neuropathology of Alzheimer's disease (AD)
- Normal changes of the aging brain
- Genetic influences on AD and normal brain aging
- Environmental exposures and the risk of AD
- AD drugs and drug trials
Talk Citation
Finch, C. (2016, May 31). Life course of the brain during normal aging and Alzheimer's disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 6, 2024, from https://doi.org/10.69645/VBOY9336.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Caleb Finch has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: Aging
Transcript
Please wait while the transcript is being prepared...
0:00
I'm Caleb Finch.
I'm a neurobiologist,
PhD at the University of Southern California.
My talk will be on the "Life Course of the Brain
during Normal Aging and Alzheimer's Disease".
I hope to bring to your attention changes
that begin relatively early and are benign as they're
understood and may progress in some individuals
to the devastating endpoints of Alzheimer's disease.
0:28
The next slide shows a truly remarkable woman,
unique in her lifespan of 122 years
and unique also in reaching that advanced age with few,
if any signs of mental deterioration.
This is Jeanne Calment and there's no one who has approached her lifespan since.
The sad fact is that about 50 percent of centenarians are mentally impaired.
0:59
The next slide shows the devastating reality
that after the age of 60 in all human populations,
the risk of Alzheimer's increases exponentially.
The risk doubles every five years after the age of 60.
That curve has a horrible prediction
that if you live long enough, you'll get Alzheimer's.
This is obviously not the case for some individuals seem to be protected.
We want to understand that.
1:32
The three larger processes that are ongoing with aging.
The best understood is infarcts or blood clots in the brain that
happen at some degree of randomness in
different parts of the brain and are associated with hypertension.
They are also on a much smaller scale in some people and those are called microinfarcts,
and of course the familiar extreme is stroke.
This is a process that is added onto
two other processes that are concurrent in almost everyone.
The largest red circle is primary neurodegeneration,
which arises during Alzheimer's disease and Parkinson's.
Then intersecting as a risk factor is damage to the white matter,
the myelin of our brain,
which has many different causes.