Ch.8 Adult & Aging Brain

THE ADULT BRAIN

Size & composition
- Loses gray matter through synaptic pruning; rate slows by late 20s
- Gains white matter through myelination; peaks ~40 yrs
- Shift from locally-organized childhood networks ➔ widely distributed adult networks
Prefrontal Cortex (PFC)
- Last major region to become fully “wired”
- Governs planning, problem-solving, decision-making, cognitive control (impulse suppression)
- Adult wiring ➔ decisions less dominated by emotion/reward/social pressure
Intelligence trajectories
- Overall peak: early–middle adulthood (≈ 25–60 yrs)
- Fluid intelligence (pattern-finding, novel problem-solving): peaks ≈ 30
- Crystallized intelligence (vocabulary, factual knowledge): rises until ≈ 50
- No single age maximizes every cognitive skill

Aging = dynamic, gradual; can feature resilience & health
Normal aging ≠ dementia/pathology
- Dementia: cognitive decline that interferes with daily life
- Profound, widespread neuron loss is pathological, not normal
Healthy aging research examines lifestyle (diet, exercise, etc.) that supports cognition

Memory
- Declarative (episodic + semantic): declines
- Non-declarative (procedural): largely spared
- Working memory: capacity & manipulation efficiency fall; decline may start ~30
Fluid-intelligence components
- Processing speed ↓
- Problem-solving agility ↓
Attention
- Selective attention: harder to filter distractions (e.g., noisy restaurant)
- Divided attention: multitasking (talking while driving) more challenging

Global brain volume
- Starts decreasing in 30s–40s; accelerates ≈ 60
Regional shrinkage (greatest ➔ lesser)
- PFC, cerebellum, hippocampus show biggest losses
Neuron-level contributors
- Smaller soma, dendritic retraction, myelin loss
- Contrasts with adolescence where volume loss = pruning + cell death
Cortical thinning
- Follows volume pattern; frontal & temporal lobes thinnest
- “Last-in, first-out” theory: regions that mature last deteriorate first
White-matter trajectories
- Projection fibers (early-maturing) age better
- Association fibers (late-maturing, intra-hemispheric) deteriorate fastest

Dendritic alterations
- Branch complexity ↓; dendritic spines lost, esp. “thin” spines (highly plastic)
- Potential link to working-memory decline (unconfirmed)
Neurogenesis
- Continues life-long in olfactory bulbs & dentate gyrus, but rate ↓ with age (steep in mice; moderate decline in humans)
- Enhancement strategies boost cognition in rodents

Neurotransmitters
- Dopamine synthesis ↓; fewer receptors ➔ impacts motivation, cognition
- Evidence suggests serotonin may also ↓

Gene-expression shifts
- Synaptic-plasticity genes under-expressed; exhibit more DNA damage
Oxidative stress & DNA damage
- Mitochondria produce free radicals → damage lipids, proteins, DNA
- Antioxidant defenses weaken with age
- Observed ↑ mitochondrial DNA damage in aging & Alzheimer’s brains; rodent oxidative damage correlates with memory impairments
- Brain uses ≈ 20\% of body’s energy ➔ high metabolic vulnerability; glucose uptake & mitochondrial efficiency decline
Immune dysfunction
- Microglia become hyper-reactive: chronic inflammation, ↓ anti-inflammatory factors, synapse remodeling deficits
- Excessive microglial activity linked to cognitive impairments in mice
Impaired protein recycling
- Autophagy & proteasome systems less efficient ➔ abnormal protein accumulation
- Neurons’ long lifespan (limited replacement) amplifies vulnerability
Systemic contributors
- Cardiovascular deterioration may drive/accelerate neural aging changes

Diet
- Cardiovascular risk factors (hypertension, high LDL) ⇒ cognitive risk
- Plant-rich diets (Mediterranean, DASH) correlate with lower dementia incidence
- Specific nutrients: antioxidants (vitamins C & E, flavonoids), omega-3 fatty acids show observational benefit; supplement trials yield mixed results
- Caloric restriction (energy intake ↓ without malnutrition) linked to cognitive benefits & longevity
Exercise
- Aerobic activity improves learning, memory, slows dementia progression, reduces cortical thinning & hippocampal shrinkage
- Mechanisms: ↑ neuroplasticity, ↑ neurogenesis, ↑ neurotrophic factors, better cerebral blood flow
- Rodent evidence: running wheels → higher hippocampal neurogenesis + better memory
- Earlier adoption likely yields stronger neuroprotection, but late-life start still beneficial
Mental stimulation & social engagement
- Enriched environments in mice (toys, mazes, social interaction) → better late-life cognition, ↑ neurogenesis, ↑ neurotrophic factors
- Humans: cognitively demanding jobs, reading, puzzles, music correlate with reduced cognitive decline
- Large social networks/active social life bolster cognition

Aging brain’s plasticity suggests interventions (lifestyle, societal supports) can meaningfully extend cognitive health span
Ethical dimension: ensuring equitable access to exercise facilities, nutritious foods, social opportunities for older adults
Public-health planning: anticipate diverse aging trajectories; distinguish normal decline from pathological dementia for early detection & resource allocation
Lifelong perspective: neuroprotective habits adopted in youth/midlife compound benefits, reinforcing preventive-medicine paradigms

Peak white-matter volume: ≈ 40 yrs
Adult intelligence peak range: 25–60 yrs; fluid \approx 30, crystallized \approx 50
Brain consumes 20\% of total body energy

Chapter 4 memory taxonomy: declarative vs. non-declarative informs aging-memory patterns
Chapter on myelination: same principles explain white-matter growth & later degeneration
Neuroplasticity concept underlies benefits of exercise, cognitive stimulation

Maturation continues into third decade; decline begins subtly by fourth
Normal aging entails selective, not wholesale, neuronal/synaptic loss
Lifestyle plays decisive role in modulating trajectory; brain health is malleable across lifespan