Journal of Behavioral and Brain Science, 2011, 1, 57-68
doi:10.4236/jbbs.2011.12008 Published Online May 2011 (http://www.scirp.org/journal/jbbs)
Dyscirculatory Angiopathy of Alzheimer’s Type
Ivan V. Maksimovich
Clinic of Cardiovascular Diseases named after Most Holy John Tobolsky, Moscow, Russia
Received March 15, 201 1; revised March 30, 2011; accepted April 2, 2011
Abstract
Purpose: We assess the significance of dyscirculatory angiopathy of Alzheimer’s type (DAAT) in identify-
ing the predisposition to the development and diagnosis of Alzheimer’s disease (AD) different stages. Meth-
ods: 108 patients took part in the research:1) 49 aged 34-79 suffering from AD or running an increased risk
of its development (those not diagnosed with AD but having growing memory disorders without any mani-
festations of dementia or specific cognitive impairments, and having 2 or more immediate relatives with AD)
- Test Group; 2) 59 aged 28-78 suffering from different types of brain lesions accompanied by dementia but
not suffering from AD or corresponding to their age norm - Control Group. All the patients underwent MRI,
CT with subsequent calculation of the temporal lobes atrophy degree, brain scintigraphy (SG), rheoencepha-
lography (REG), and MUGA. Results: Characteristic features of patients with an increased risk of AD as
well as at its various stages are: 1) Temporal lobes and hippocampus atrophy ranging from 4% among those
with an increased risk of AD to 62% among those at its advanced stages; 2) DAAT manifestations: reduction
of the capillary bed in the temporal and frontoparietal regions with the development of multiple arterioven-
ous shunts of the same localization and correspondent early venous discharge accompanied by venous stasis
on the border of the frontal and parietal region; 3) DAAT phenomena equally develop both among those with
an increased risk of developing AD and those at various AD stages. Similar changes are not observed among
Control Group patients with other brain lesions, regardless of the severity of dementia, as well as among
practically healthy people of the corresponding age group. Conclusion: Timely identification of the above-
mentioned changes can reveal a predisposition to AD development long before its initial manifestations, and
it allows differentiating AD from other diseases attended by dementia. In both cases, timely diagnosis allows
beginning timely treatment and thus achieving more stable results.
Keywords: Alzheimer’s Disease, Dementia, Hippocampus, Temporal Lobes Atrophy, Dyscirculatory
Angiopathy of Alzheimer’s Type
1. Introduction
Alzheimer’s disease (AD) is becoming more widespread
each year. According to the Alzheimer’s Association, in
2007, 5.1 million cases were registered only in the United
States [1]. In 2009, the number of cases increased to 5.3
million [2], and in 2050 it will approximately increase to
13.5 million [3]. In 2010, there were 35.6 million pa-
tients around the world, and it is estimated that by 2050
this figure will approach 115.4 million [4]. It all suggests
that AD is becoming a global problem of mankind. One
of the important issues in solving this problem is early
diagnosis of the disease and timely visualization of
changes and processes in the brain during disease devel-
opment [5]. Another issue of no less importance is the
differentiation of AD from other diseases that are char-
acterized by the development of dementia [6-8].
A great step in the diagnosis of AD was the introduce-
tion of CT and MRI which made it possible to visualize
the brain and to detect changes developing in the tissues
of the temporal lobes and the hippocampus [9-12].
However, using standard CT or MRI techniques does not
always allow differentiating AD from other diseases as-
sociated with dementia [13]. The introduction of PET has
made it possible to carry out not only structural but also
functional studies of the hippocampus [14-17] which
consequently led to the development of fairly complex
integrated visualization techniques [18]. The next achie-
vement in AD diagnosis was the emerging of biomarkers
and the development of various methods of their use, but

58 I. V. MAKSIMOVICH
this extremely promising research is still under study
[19].
There are certain problems in the diagnosis of early
stage disease accompanied by mild dementia and Mild
Cognitive Impairment (MCI) [16,17]. It is even more
difficult to diagnose pre-clinical stages when the disease
has not yet developed, there are no manifestations of
dementia, and its development is only probable [13,19,
20].
Despite the fact that it was in the 1930s when F. Morel
found out that AD was accompanied by dysoric or dru-
soidal angiopathy, the state of the brain vascular system
in Alzheimer’s disease has received insufficient attention.
Until recently, medical literature had only some isolated
reports on this subject [21-24]. The research was mostly
carried out by means of ultrasound and MRI techniques
which did not always give a clear picture. Accordingly,
hemodynamic changes of the brain [25] and the devel-
opment of perfusion abnormalities [26,27] have been
looked at from the function al side to a greater ex tent, and
vascular disorders were seen in terms of location of amy-
loid deposits and amyloid angiopathy [28-30], but not in
terms of vascular pathology. Visualization of arte- rial,
capillary and venous blood flow of the brain, as well as
their correlation in AD, has yet received insufficient at-
tention.
2. Materials and Methods
The whole research was made with the approval of the
Ethics Committee and with the consent of the examined
patients and their relatives. Our objective was to identify
specific structural defects and their correlation with an-
gioarchitectonic changes appearing in the brain during
AD development, as well as the identification of these
changes among patients with a predisposition to AD de-
velopment, and their comparison with cerebral and cere-
brovascular changes that occur in the control group of
patients of the same age who suffer from other lesions of
the brain accompanied by the development of dementia
or not accompanied by the development of dementia. To
carry out complete differential diagnosis of all the pa-
tients was not the objective of this research .
108 patients aged from 28 to 79 (average age 67) were
examined during the research.
The Test Group included 49 patients aged from 34 to
79 (average age 65), 18 men (36.7%) and 31 women
(63.3%).
43 patients suffering from AD were subdivided ac-
cording to one of the most common classifications pro-
posed by J. C. Morris in 1993 (The Clinical Dementia
Rating /CDR/) [31]:
 CDR-1 - Group with mild dementia, mild cognitive
impairment, had previously been diagnosed AD,
medical history did not exceed 2 years - 15 (30.6%)
patients;
 CDR-2 - Group with moderate dementia, quite per-
sistent cognitive impairment, had previously been
diagnosed with AD, history of the disease ranged
from 2 to 6 years - 20 (40.8%) patients;
 CDR-3 - Group with fairly severe dementia, gross
cognitive impairment, had previously been diag-
nosed with AD, history of the disease ranged from 7
to 15 years - 8 (16.3%) patients;
 A separate group of 6 (12.2%) included the patients’
relatives with a high risk of developing the disease
who wished to have an examination. They were all
fairly young, aged from 34 to 42, had growing
memory disorders without any manifestations of
dementia or any specific cognitiv e impairment.
The Control Group included 59 patients aged from 28
to 78 (average age 68), 36 (61.0%) men and 23 (39.0%)
women.
Control Group patients either had different types of
brain lesions with varying degrees of severity accompa-
nied by signs of dementia and cognitive impairment, but
did not suffer from Alzheimer’s disease or considered
themselves healthy; they did not have any specific com-
plaints and their brain changes were seen as age-corre-
sponding and normal.
Those patients were divided into the following groups:
 A group at the initial stage of chronic cerebrovas-
cular insufficiency of atherosclerotic genesis with-
out any signs of dementia or cognitive impairment;
usually those patients, regardless of age, had some
complaints which were considered normal taking
into account age-related changes of the brain - 17
(28.8%) pat ie n t s;
 A group with sufficiently severe chronic cere-
brovascular insufficiency of atherosclerotic genesis
without gross occlusive vascular lesions; they had
incipient mild dementia and initial cognitive im-
pairment - 12 (20.3%) patients;
 A group with multiple atherosclerotic lesions of the
brain, severe vascular dementia and cognitive im-
pairment, with a history of recurrent small focal
strokes - 6 (10. 2%) pati e nt s;
 A group with atherosclerotic (vascular) Parkinson-
ism and signs of dementia - 14 (23.7%) patients;
 A group with Binswanger's disease and manifesta-
tions of dementia - 6 (10.2%) patients;
 A group with Parkinson’s disease and manifesta-
tions of dementia 4 (6.8%) patients.
The research plan included: computed tomography of
the brain (CT), magnetic resonance imaging (MRI), scin-
tigraphy of the brain (SG), rheoencephalography (REG),

I. V. MAKSIMOVICH
59
multi-gated angiography (MUGA).
CT was preferred over MRI in the research, as it was
necessary to better visualize calcium deposits in the vas-
cular wall in atherosclerotic lesions and to identify the
nature of vascular pathology. The main goal of the re-
search was study of the changes in the temporal lobes
and the hippocampus, as they are the first to suffer from
the development of AD [9-12,16,17], as well as the fact
that they are easily enough visualized on the scans by
bone forma ti o ns.
CT of the brain was performed on apparatus “Soma-
tom” (Siemens), “HiSpeed” (GE), “Tomoscan” (Philips)
by the following procedure: the patient was placed ac-
cording to the classical pattern, the boundary of the first
scan took place on the orbital-miotal line, producing
scans 2.5 mm thick with an interval of 2.5 mm. The
boundaries of cerebral fosses on both sides were ascer-
tained by bone marks. A consistent two-side measure-
ment of cerebral fosses region and measurement of the
size of the substance of the right and left temporal lobes
of the brain for each scan were made with computer pro-
gram “Advanced Tomo Area Analysis” (ATAA). Next,
the area of the lower horn of lateral ventricle and the area
of the sulci were subtracted and then compared with the
area of the corresponding cranial fossa at the same level.
The ratio of these quantities makes it p ossible to compare
the state of brain tissue both in its normal condition and
during the development of atrophic process. Reduction
of the size of the brain tissue area at each scan corre-
sponds to the severity of atrophic changes at this brain
level. Then the above mentioned quantities were auto-
matically recalculated by the thickness of each scan and
each interval between the scans, and the volume of the
right and left temporal lobes of the brain was determined,
and thus the mass of brain tissue in the surveyed areas
was calculated. Next, the masses of tissue of left and
right temporal lobes were summed up. The results of the
research automatically showed both the normal amount
of tissue for the corresponding age group and the per-
centage decrease of the volume of the temporal lobes of
the brain. The percentage ratio of those values deter-
mined the severity of atrophic changes in the temporal
regions of the brain and, consequently, in the hippocam-
pus tissue [12,32]. The data showed a tendency to de-
velop Alzheimer’s disease or the stage of its develop-
ment in the experimental group and also pointed at the
pres- ence or absence of atrophic changes in the temporal
lobes of the brain in the control group of patients.
Due to the fact that examined patients belonged to
different age groups, the study took into account
age-related changes in brain tissue [32,34]. For example,
the fact that patients aged 60 and older had common
atrophic changes of the brain, along with a decrease of
the size of the temporal lobes of up to 5%, was regarded
as natural age-related changes and equal to normal [33].
SG of the brain was carried out on a gamma camera
(Ohio Nuclear, U.S.) following the classical method in
dynamic and static mode using the TC 99M pertechnetat
555.
REG was conducted by means of “Reospektr-8”
(Neurosoft, Russia) in accordance with the standard
automated method with the determination of pulse vol-
ume abnormalities.
MUGA of the brain was performed on apparatus
“Advantx” (GE) following the classical method of trans-
femoral access. 10 - 12 ml of Omnipack 350 was intro-
duced intra-carotidally and 7 - 8 ml intra-vertebrally.
Registration was carried out in direct and side projec-
tions in constant subtraction mode at a speed of 25
frames per second.
3. Results
Since all classifications of stages and types of AD are
functional in nature [6,8,18] and are not based on mor-
phological changes, we have slightly modified the pre-
viously used classification proposed by J. C. Morris (The
Clinical Dementia Rating) [31] and added a morpho-
logical component to it. Thus, the patients were divided
into groups in accordance with the degree of severity of
atrophic changes in the temporal lobes of the brain, as
well as the degree of severity of dementia, cognitive im-
pairment and the severity and duration of the disease.
Analyzing the results obtained, we introduced Group
CDR-0 (as opposed to the method proposed by J. C.
Morris where the earliest stage was represented by
Group CDR-0,5). In our research, this group included
relatives of patients with AD, i.e. people aged from 34 to
42 who had not been diagnosed with AD but who had
growing memory disorders without any manifestations of
dementia or any specific cognitive impairment and who
had 2 or more immediate relatives suffering from AD.
These patients were identified as a group running a high
risk of acquiring the disease or a group with a possibility
of its inheritance.
In the Test Group of patients, CT revealed the follow-
ing main types of changes in brain tissue (Table 1):
 In Group CDR-0: 4 (66.6%) patients had atrophy of
the temporal lobes of the brain with a decrease of
tissue mass of 4% - 8% (Figures 1(a), 1(b)). 2
(33.4%) patients did not have any atrophic changes
at the time of the examination, so they were with-
drawn from those wit h a possible i nheritance of AD;
 In Group CDR-1: 15 (100%) patients with mild de-
mentia, mild cognitive impairment, early clinical
stage of the disease and a history of up to 2 years
had atrophy of the temporal lobes with a decrease of

60 I. V. MAKSIMOVICH
tissue mass of 9% - 18% (Figures 2(a), 2(b));
 In Group CDR-2: 20 (100%) patients with moderate
dementia, persistent cognitive impairment, middle
clinical stage of the disease and a hi story of 2 to 6 y ears,
had atrophy of the temporal lobes with a decrease of
tissue mass of 19% - 32% (Figures 3(a), 3(b)).
 In Group CDR-3: 8 (100%) patients with severe
dementia, gross cognitive impairment, late-stage
clinical AD and a history of 6 to 15 years had gross
atrophy of the temporal lobes accompanied by a de-
Figure 1. Tomograms of patient P. (36 years old, fe-
male) with an increased risk of AD development. (a)
7% atrophy of the right temporal lobe (zones 1 - 4); (b)
8% atrophy of the left temporal lobe (zones 1 - 3). Ar-
rows indicate dilation of Sylvius fissure and subar-
obchnoidal space.
Figure 2 Tomograms of patient S. (42 years old,
male); 2-year anamnesis of the disease. (a) 18% at-
rophy of the right temporal lobe (zones 1 - 4); (b)
17% atrophy of the left temporal lobe (zones 1 - 4).
crease of tissue mass of 33-62%; in some cases those
changes were accompanied by formation of rather
extensive cavities in th e tissue (Figures 4(a), 4( b)).
Simultaneously, patients of the Test Group had the
following:
 Absence or insignificant amount of calcium salts
deposits in the walls of cerebral vessels - 47 (100%)
patients;
 Dilation of Sylvian fissure (Figures 1-4) associated
with atrophic changes, mainly of the temporal and
partially frontal lobes of the brain - 47 (100%) pa-
tients;

I. V. MAKSIMOVICH
61
Figure 3. Tomograms of patient T. (58 years old, male);
6-year anamnesis. (a) 20% atrophy of the right tem-
poral lobe (zones 1 - 9); (b) 22% atrophy of the left
temporal lobe (zones 1 - 11). Arrows indicate dilation
of Sylvius fissure and subarochnoidal spac e .
 Local involutive changes of the cerebral cortex as-
sociated with the dilation of the sulci of up to 1.5 -
5.0 mm, and dilation of subarachnoid space of con-
vexital surfaces of the temporal and fron-
tal-parietal regions - 47 (100%) patients;
 General invalutive changes of the cerebral cortex -
18 (38.3%) patients;
 Signs of unocclusive hydrocephalus - 29 (61.7%)
patients;
CT revealed the following features of Control Group
Figure 4. Tomograms of patient S. (67 years old, male);
12-year anamnesis. (a) 41% atrophy of the right tem-
poral lobe (zones 1 - 5); (b) 62% atrophy of the left
temporal lobe (zones 1 - 5).
patients’ b ra i n tissue (Table 1):
 Local atrophic changes in the temporal lobes were
not detected in any case;
 General atrophy of the brain among patients aged
from 60 to 78 accompanied by atrophy of the tem-
poral lobes, with a decrease of tissue mass of 5%
(which corresponds to the age norm), were detected
among 26 (44.1%) patients [33];
 Multiple calcium deposits in the walls of intracra-
nial vessels - 55 (9 3. 2%) patients;
 Dilation of Sylvian fissure associated with general

I. V. MAKSIMOVICH
62
atrophic chang es - 41 (6 9. 5%) patients;
 General involutive changes of the cerebral cortex
associated with the dilation of the sulci of up to 1.5
- 2.0 mm, and dilation of subarachnoid space of
convexital surfaces - 35 (59.3%) patients;
 Signs of unocclusive hydrocephalus - 35 (59.3%)
patients.
Simultaneously, Control Group patients had the fol-
lowing:
 Single postischemic macrocysts (5 - 10 mm) – 7
(11.9%) pat ie n t s;
 Single postischemic microcysts (3 - 5 mm) – 25
(42.4%) pat ie n t s;
 Multiple postischemic microcysts (3 - 5 mm) – 9
(15.3%) pat ie n t s;
 Manifestations of leucoaraiosis – 18 (30.5%) pa-
tients.
In the Test Group, SG showed blood flow slowdown
in the cerebral hemispheres of up to T max 9 - 10 s., T
1/2 10 - 11 s. in 31 (66.0%) cases, of up to T max 12 - 13
s., T 1/2 15 - 20 s. – in 16 (34.0%) cases.
In the Control Group, according to SG, blood flow
slowdown in the cerebral hemispheres of up to T max 10 -
12 s., T 1/2 11 - 13 s. was ob served in 37 (62.7%) cases, of
up to T max 14 - 15 s., T 1/2 15 - 20 s. – in 22 (37.3%)
cases.
In the Test Group REG showed a decrease in pulse
blood filling volume in the caro tid system of 15% - 20%
in 28 (59.6%) cases, 40% - 50% – in 19 (40.4%) cases.
In the Control Group, according to REG data, a de-
crease in pulse blood filling volume in the carotid system
of 20-35% was detected in 35 (59.3%) cases, of 45% -
60% – in 24 (40.7%) cases.
MUGA in the Test Group revealed (Table 2):
 Absence (or they were poorly expressed) of athero-
sclerotic changes of extra and intracranial arteries -
47 (100%) patients;
 Increased looping of the distal branches of intracra-
nial arteries - 37 (7 8.7%) patients (Figure 5);
 Reduction of capillary contrast phase in a cone-
shaped microvascular area in the frontoparietal re-
gions and the projection of the hippocampus - 47
(100%) patients (Figure 6);
Table 1. CT data obtained by means of ATAA program.
Signs Test group
(Alzheimer’s disease)Control group (brain disor ders other than Alzheimer’s disease) p (chi-square)
Number of patients 47 59
Multiple calcium salt deposits on the walls of intracranial
vessels 0 55 < 0.005
Scattered postischemic macr ocysts (5 - 10 mm) 0 7 0.015
Scattered postischemic microcysts (3 - 5 mm) 0 25 < 0.005
Multiple postischemic microcysts (3 - 5 mm) 0 9 0.0051
Manifestation of leucoaraiosis 0 18 < 0.005
Reduction in the size of the temporal lobes of the brain of 4
to 8% 4 0 0.022
Reduction in the size of the temporal lobes of the brain of 0
to 5% among patients older tha n 60 0 26 < 0.005
Reduction in the size of the temporal lobes of the brain of 9
to18% 15 0 < 0.005
Reduction in the size of the temporal lobes of the brain of 19
to 32% 20 0 < 0.005
Reduction in the size of the temporal lobes of the brain of 33
to 65% 8 0 < 0.005
Dilation of Sylvius fissure 47 41 < 0.005
Local involutive changes of the cerebral cortex in the tempo-
ral regions of the brain 47 0 < 0.005
General involuntary changes in the cer e bral cortex 18 35 0.031
Signs of nonocclusive hydrocephaly 29 35 0.803 (no)
The differences between the groups were identified by the analysis of the relevant contingency tables 2 × 2 by means of Pearson’s chi-square tes t. The corre-
sponding val ues of p are shown in the last column of the table. P-value = 0.05”.

I. V. MAKSIMOVICH
63
1. Multiple loop formation; 2. Multiple arteriovenous shunts in
frontoparietal and temporal regions; 3. Development of hypo-
vascular region.
Figure 5. Angiogram of the left internal carotid of a
67-year old patient (12-year anamnesis); side projec-
tion; arterial opacification phase.
1. Multiple arteriovenous shunts; 2. Reduction of capillary
opacification in the form of hypovascular zone in the frontopa-
rietal and temporal regions.
Figure 6. Angiogram of the left internal carotid of a
56-year old patient (7-year anamnesis); side projection;
capillary opacification phase.
 Multiple arteriovenous shunts in the region of the
arterial branches supplying the frontoparietal cor-
tex, and in the region of the anterior choroid artery
supplying the hippocampus, accompanied by early
venous shunts - 47 (100%) patients (Figures 6, 7
and 8).
1. Multiple arteriovenous shunts; 2. Development of hypo-
vascular region.
Figure 7. Angiogram of the right internal carotid of
a 40-year old patient (2-year anamnesis); side pro-
jection; capillary opacification p h ase.
1. Multiple a rteriovenous shunts.
Figure 8. Angiogram of the right internal carotid of a
34-year old patient (high-ri sk group); side projection;
late arterial opacification phase.
 Anomalous venous congestion at the border of fron-
tal and parietal lobe - 43 (91.5%) patients (Figure 9,
10);
 The development of abnormal lateral veins in the
frontoparietal region - 42 (89.3%) patients (Figure
11, 12).
MUGA in the Control Group revealed (Tab le 2):
 Atherosclerotic changes in intra- and extracranial
vessels - 57 (96. 6 %) pati e nt s;

64 I. V. MAKSIMOVICH
1. Development of anomalous venous trunks in the frontoparietal
region.
Figure 9. Angiography of the right internal carotid of
a 34-year old patient (increased risk of AD develop-
ment); side projection; venous opacification phase.
1. Development of anomalous venous trunks in the frontoparietal
region.
Figure 10. Angiography of the left internal carotid of a
75-year old patient (15-year anamnesis); side projec-
tion; venous pacification phase.
 A tendency towards increased looping of distal
branches - 3 (5.1%) patients;
 Reduction of capillary contrast phase in the fronto-
parietal regions and hippocampus projection with
formation of hypovascular zones was not detected
in any case;
 Local arteriovenous shunts in the frontoparietal and
1. Development of congestion on the boundary of the frontoparietal
region.
Figure 11. Angiography of the right internal carotid of a
34-year old patient (increased risk of AD development);
side projection; venous opacification phase.
1. Development of congestion on the boundary of the frontopa-
rietal region.
Figure 12. Angiography of the left internal carotid in
75-year old patient (12-year anamnesis); side projec-
tion; venous opacification phase.
temporal regions were not revealed in any case;
 Early venous discharge in the frontoparietal and
temporal regions were not iden tified in any case;
 Existing arteriovenous shunts were scattered in na-
ture, located at the level of the white substance of
the brain and detected in 27 (45.8%) cases;

I. V. MAKSIMOVICH
65
Table 2. MUGA data.
Signs Test group (Alzheimer’s
disease) Control group (brain disorders other than Alzheimer’s disease) p (chi-square)
Number of patients 47 59 < 0.005
Atherosclerotic changes 0 57 < 0.005
Increased looping in distal regions of intracranial ves-
sels 37 3 < 0.005
Reduction of capillary blood flow in frontoparietal
region 47 0 < 0.005
Multiple arteriovenous shunts infrontoparietal and
temporal regions 47 0 < 0.005
Multiple scattered arteriovenous shunts at the level of
the white substance of the bra in 0 27 < 0.005
Premature venous shunts in frontoparietal and temporal
regions 47 0 < 0.005
Scattered premature venous shunts 0 28 < 0.005
Venous congestion on the boundary of frontal and
parietal regions 43 0 < 0.005
Development of anomalous lateral veins in parietal
region 42 0 < 0.005
The differences between the groups were identified by the analysis of the relevant contingency tables 2 × 2 by means of Pearson’s chi-square tes t. The corre-
sponding val ues of p are shown in the last column of the table. P-value = 0.05”.
 Early venous shunts were diffuse in nature depend-
ing on the localization of arteriovenous shunts and
were detected in 28 (47.5%) cases;
 Anomalous venous congestion at the border of
frontal and parietal lobe was not detected in any
case;
 Anomalous lateral veins in the frontoparietal region
were not detected in any case;
Specific disorders of blood circulation and microcir-
culation in the hippocampus and frontoparietal cortex
revealed among patients of the Test Group were named
the “dyscirculatory angiopathy of Alzheimer’s type” [33].
Interestingly, the severity of these disorders does not
depend on the timing of the development of AD symp-
toms and severity of dementia, it is almost equally ob-
served both among those running a risk of developing the
disease and groups at its early and late clinical stages.
4. Discussion
The data obtained show that examined patients of the
Test and Control Groups have clear differences of mor-
phological and structural defects, as well as changes in
angioarchitectonics and microcirculation in the brain.
Patients running a high risk of acquiring AD, as well
as patients at different stages of the disease ranging from
early to late ones have specific structural changes of at-
rophic character developing in the temporal lobes of the
brain.
These changes are characterized by a decrease in pulp
tissue of the temporal lobes and the hippocampus of 4% -
62% [10,12]. At early stages it is manifested in re- gional
atrophy, and at late ones, atrophy leads to forma- tion of
cavities. Besides, these changes are accompanied by lo-
cal dilation of Sylvian fissure and subarachnoid space
due to atrophy of the temporal and frontal lobes [13,16].
The degree of these changes is directly depend- ent on
the stage of disease, the severity of dementia, and cogni-
tive disorders [11,18,19].
Similar atrophic changes, localized in the temporal
lobes of the brain, do not occur among patients of the
Control Group with other lesions of the brain accompa-
nied by the manifestations of dementia; similarly, they
do not occur among patients of the Control Group who
correspond to their age norm.
Simultaneously, AD leads to the development of some
specific cardiovascular and microcirculatory abnormali-
ties in the brain which we have named dyscirculatory
angiopathy of Alzheimer’s type [33]. These abnormali-
ties are characterized by increased looping in the distal
parts of intracranial arteries, reduction of capillary blood
flow in the frontoparietal and temporal regions with the
formation of hypovascular zones [22,32], the develop-
ment of multiple arteriovenous shunts in the same brain
regions. These changes lead to local early venous shunts
and to simultaneous venous congestion on the border of
the frontal and parietal regions [21,24]. The venous con-
gestion is caused by impaired blood flow from the tem-
poral and frontal-parietal regions which are caused by
the reduction of the capillary bed. In turn, this leads to
the formation of specific abnormal venous trunks [32].
All these changes lead to failure of bloo d supply in the

66 I. V. MAKSIMOVICH
abovementioned brain regions and, consequently, to spe-
cific microcirculatory hypoperfusion [25,26] that may
contribute to the deposition of abn ormal proteins in brain
tissue or the violation of their removal [28,29].
There is an opinion that at early stages of AD hyper-
perfusion occurs in the frontoparietal and temporal brain
regions against the background of hypoperfusion [27].
These data were obtained in MRI studies. In fact, the
authors observed no true hyperperfusion but an active
discharge of blood through arteriovenous shunts which is
a consequence of hypoperfusion caused by reduction of
capillary blood flow.
We cannot exclude that the lesion of microvascular
bed is associated with the symptoms of amyloid an-
giopathy and Morel’s angiopathy [28], or possible
paravasal amyloid deposits [21,23]. However, the dis-
circulatory violations identified in the research affect not
only the capillaries as they were described by F. Morel,
but also arteries and veins. The severity of these abnor-
malities does not dep end on the timing of sympto ms, the
severity of dementia or cognitive disorders. These ab-
normalities are observed both among patients running a
high risk of acquiring the disease who have no clinical
symptoms and among patients at early and late clinical
stages of AD. This fact does not allow stating with cer-
tainty that the development of AD begins with amyloid
deposition in the vascular wall, and only then its deposi-
tion in the brain tissue begins [24,33,35].
As a result, the question of what is primary arises: if it
is congenital, or by some reason acquired, disorders of
blood circulation and microcirculation that promote the
development of AD, or if it is the disease itself that
causes similar changes of the distal arterial, microcircu-
latory and venous bed in the brain [33]?
Atherosclerotic changes of intracranial blood vessels
accompanied by calcium deposits in the walls of the ar-
teries, the development of stenotic and occlusive lesions
causing ischemic manifestations with the development of
micro-and macro-cysts and the phenomena of leu-
coaraiosis are not characteristic for AD and practically
never occur [24,33]. These changes with varying but
high enough frequency and severity are found in the
Control Group both among patients who correspond to
their age norm and among those suffering from other
types of atherosclerotic lesions, vascular dementia or
Binswanger’s or Parkinso n’s disease [33,36].
Control Group patients hardly ever have increased
looping of distal intracranial arteries, or it is quite rare
(5.8%) [13]. Besides, they do not have local reduction of
the capillary bed with the depletion of the capillary b loo d
flow in the temporal and frontoparietal regions with the
formation of hypovascular zones in the same regions.
Early arterioven ous shunts do occur among patien ts of
the Control Group, but they are not localized in the fron-
toparietal and temporal regions being scattered at the
level of the white substance of the brain, and early ve-
nous discharge occurs in the same regions. Neither did
patients of the Control Group have any marked venous
stasis [33].
General changes among patients of Test and Control
Groups are the signs of nonocclusive hydrocephaly and
general atrophy of the cerebral cortex which are
age-characteristic [34].
The research conducted has shown that such common
and simple methods as SG of the brain and REG have
their own place in the diagnosis of AD, but they prove
not to be sufficiently effective for the differentiation
from other pathological conditions of the brain.
On the contrary, CT combined with ATAA program
and MUGA of the brain makes it possible to achieve
significant results in diagnosing the disease. It is inter-
esting to note that the use of CT, unlike MRI, is more
promising as it provides a better opportunity to visualize
calcium deposits in atherosclero tic tissues which to some
extent allows differentiating the nature of the vascular
lesion.
5. Conclusions
AD is characterized by a specific number of structural
brain disorders which includes morphological changes of
atrophic nature developing in the temporal lobes of the
brain and the hippocampus, as well as violations in an-
gioarchitectonics and microcirculation. These can be
divided into the following sections:
1. Atrophic p h e nomena:
 Atrophy of the temporal lobes of the brain and the
hippocampus reaching in some cases up to 62%;
 Dilation of Sylvian fissu re mainly due to atrophy of
the temporal lobes;
2. The phenomena of dyscirculatory angiopathy of
Alzheimer’s type:
 Reduction of the capillary bed in the temporal and
frontal-parietal regions of the brain;
 The development of multiple arteriovenous shunts
in the same regions;
 Early venous discharge in the same regions;
 Venous stasis with the development of abnormal
venous trunks on the border of the frontal and pa-
rietal region;
 Large looping of the distal branches of intracranial
arteries.
These changes can be traced not only among patients
at advanced stages of the disease but also among those at
its earliest and preclinical stages. Timely detection of
these changes is of great importance for examining pa-

I. V. MAKSIMOVICH
67
tients with a high risk of acquiring AD and patients at
early clinical stages, as it will make it possible to begin
treatment sooner and thus achieve more pronounced and
persistent results. Besides, detecting these changes is
important for the differentiation of AD from other patho-
logical cond itions of the brain accompanied by co gnitive
impairment and dementia.
A combination of CT of the brain with ATAA pro-
gram and cerebral MUGA can quite easily be used in a
modern hospital, and they have a low cost.
A relative disadvantage of the proposed method is the
usage of a fairly complex invasive multi-gated an-
giography (MUGA) requiring a percutaneous arterial
puncture, catheterization of carotid and vertebral arteries
with subsequent introduction of radiopaque substance.
MUGA is the “golden standard” for diagnosis of the
brain vascular system yet. However, in future, improved
CT, MRI and PET will allow receiving high-quality,
high-resolution angiog raphic images of arterial, capillary
and venous contrast phases by means of less invasive and
simpler and more benign methods.
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