1. Anatomo-Histology From Table 8.10 Brain atrophy, flattening of gyri,
widening of sulci,
& cerebral ventricles
Loss of cholinergic neurons, in nucleus of Meynert, hippocampus
& association cortices
Loss of adrenergic neurons, in locus ceruleus
Denudation of neurons, stripping of dendrites, damage to axons
Increased microglia
From Table
8.10

2. Pathology
Accumulation of cell inclusions: lipofuscin, Hirano and Lewy bodies,
altered cytoskeletal
Tau proteins,
ubiquitin
Neurofibrillary tangles, neuritic plaques with amyloid,
Perivascular amyloid, distributed throughout the brain, but especially in frontal,
prefrontal lobes,
Hippocampus, 
association cortices

3. Metabolism
Decreased oxidative metabolism, slower enzyme activity (Ch. 7)
Free-radical
accumulation (Ch. 5)
Impaired iron
homeostasis (Ch. 7)
Other minerals, zinc, aluminum
Reduced level/metabolism/ activity of neurotransmitters
Increased amyloid  peptide with accumulation of amyloid proteins
Increased prion protein
Altered immune response

6. Learning at all Ages Induces Successful Aging

9. Aging of the Cardiovascular System
Chapter 16
P.S. Timiras

10. Major Functions of the Cardiovascular System
Transports O2 & nutrients to the tissues
& returns C02 to the lungs and other products of metabolism to the kidney
Regulates body temperature
Distributes hormones and other agents that regulate cell function

11. Major Components of the Cardiovascular System
Heart
Pump that circulates the blood throughout the body
Vascular System
Transports blood to the body tissues
Central Nervous System (CNS)
Particularly the centers in the medulla that regulate the function of the heart and blood vessels

13. Atherosclerosis What?

14. Arteriosclerosis: Sclerosis: hardening of the arterial wall and narrowing of the arterial lumen Atherosclerosis: Same as arteriosclerosis PLUS presence of artheroma (yellowish plaque containing lipids and cholesterol) on the arterial wall

15. Atherosclerosis Universal Progressive Deleterious Irreversible (?)

16. Fig. 16-3: Natural history of atherosclerosis
Fig. 16-3: Natural history of atherosclerosis. Pathogenesis of human atherosclerotic lesions and their clinical manifestations.

17. Myocardial Infarction

18. Stroke

19. Aneurysm

20. Atherosclerosis Affects the Arteries
Arteries: the large arteries, the arterioles, & the capillaries
See Box 16-1, Fig. 16-1, Fig (pgs )

21. Progressiveness of Atherosclerosis
Onset at young age
Progression through adulthood
Culmination in old age with overt disease manifestation
Consequences leading to severe disability & death

22. END

23. Extracellular cholesterol and cholesterol-filled macrophages (foam cells) accumulate in subendothelial space. Subsequent structural modifications of LDL particles render them more atherogenic. Oxidation of subendothelial LDL attracts monocytes, which enter subendothelium and change into macrophages. Macrophages may take up oxidized LDL to form foam cells.

24. Fibrous plaque larger than fatty streak and occupies more of the arterial lumen. Thickened cap synthesized by modified smooth muscle cells. Central core consists of extracellular cholesterol. Foam cells surrounding core derived primarily from smooth muscle cells. Fatty streaks may continue to form at periphery of plaque.

25. Total or partial occlusion of coronary artery due to plaque rupture and thrombosis can cause angina or frank myocardial infarction.
Plaques likely to rupture termed unstable. Rupture usually occurs in lipid-rich and foam cell-rich peripheral margins and may result in thrombosis and arterial occlusion.

26. Table 16-5: General Characteristics of Atherosclerotic Lesions
Early onset -- progressive
Focal lesions
Early lesions
Advance lesions
Damage, Repair, Regression
Progression of localized lesions influenced by:
Local factors: vessel structure and metabolism, blood turbulence
Systemic factors: diabetes, hypertension, stress, genetic predisposition