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

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

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

Learning at all Ages Induces Successful Aging

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

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

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

Atherosclerosis What?

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

Atherosclerosis Universal Progressive Deleterious Irreversible (?)

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

Myocardial Infarction

Stroke

Aneurysm

Atherosclerosis Affects the Arteries Arteries: the large arteries, the arterioles, & the capillaries See Box 16-1, Fig. 16-1, Fig. 16-2 (pgs. 287-289)

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

END

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.

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.

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.

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